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joepieeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeee 
wat jij wil dan
hatseeeeeeeeeeeeeeeeeeee hatseeeeeeeeeeeeee
hatseeeeeeeeeeeeee Ben weer wat kwijt.....pffff
t leven met PEP is beter vin ik dan
t leven met PEP is beter vin ik dan
ik niet
Uitspraak van [PPT] C@NDYMAN
t leven met PEP is beter vin ik dan
ik niet
ik ook nie
helemaal dol in het schedeltjuhh
ik ook nie
helemaal dol in het schedeltjuhh
zijn zat mensen die een minder mooi leven hebben door die zooi...
Zelf nog nooit gehad dus kan dr niet over oordelen.
Zelf nog nooit gehad dus kan dr niet over oordelen.
hatseeeeeeeeeeeeeee hatseeeeeeeeeeeeeeeeeeeeeeeeeeeeee
hatseeeeeeeeeeeeeeeeeeeeeeeeeeeeee
moet dat niet zijn LIJKT mooi met coke ,
cocaine running around my brain
pep is bter
lol, maar onzin.... Naar mij kennis is sos minder slecht voor het lichaam(en de rest) dan pep... das een feit. Sla de wetenschappelijke boeken maar eens open, zie onderwerp farma-toxicologie. Of het kan nog makkelijker, neem 2 biefstukkjes, leg op de een een 1/2 gr pep en op de ander 1/2 gr sos. Wacht een paar dagen en zie het resultaat....ik hoef dan niets meer verder te zeggen
PS. 1/4 gr mag ook
hahahaha jij bent echt grappig! pep is inderdaad slechter dan coke. maar coke is ook echt slecht voor je lichaam en geest!!! moet je toch nog eens proberen de echte waarheid op te zoeken! ga eens na het C.A.D. DAAR KRIJG JE FOLDERS EN DAN LEES JE MAAR EENS GOED! en dan praten we verder
hahahaha jij bent echt grappig! pep is inderdaad slechter dan coke. maar coke is ook echt slecht voor je lichaam en geest!!! moet je toch nog eens proberen de echte waarheid op te zoeken! ga eens na het C.A.D. DAAR KRIJG JE FOLDERS EN DAN LEES JE MAAR EENS GOED! en dan praten we verder
Jongen als jij nou eens zou weten waar ik werk en heb gewerkt en wat ik gestudeert heb.. zou je niet eens mij de les proberen te lezen..maar als nog lollig dat je het denkt te moeten doen..Ik heb het dus over goed gewassen sos tegenover pep... dus de verontreinigingen even er buiten laten. En dan bij een gemiddelt gebuikers partoon.
Amphetamine and methamphetamine undoubtedly cause irreversible brain damage with long-term use.
bron: Curr Opin Pharmacol. 2005 Feb;5(1):79-86.
Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK.
Tis maar wat je info vind... een folder of universitaire studie's...LMAO
t'is maar in wat voor mate je 't gebruikt, als je goeie pep lees: PERFETINE hebt en je spuit 't ist minder schadelijk dan coke snuiven.....
Perfetine is gewoon snuif Mehtamphetamine niets meer!!Is dat dan meteen goede?? nee dus!
laatste aanpassing
neem 2 biefstukkjes, leg op de een een 1/2 gr pep en op de ander 1/2 gr sos. Wacht een paar dagen en zie het resultaat....ik hoef dan niets meer verder te zeggen
Jongen als jij nou eens zou weten waar ik werk en heb gewerkt en wat ik gestudeert heb.. zou je niet eens mij de les proberen te lezen..
als je echt denkt dat je daaruit kan aflezen wat schadelijker is..
gooi maar eens een plak ham in een glas cola..
speed boven alles
Ik zie er fit uit, wanneer ik
lekker geslapen heb
lekker geslapen heb
hatseeeeeeeeeeeeeeeee
laatste aanpassing
donateur
het leven is pas mooi als je kan genieten van iets zonder coke
coke is verloederd
coke is verloederd
CoKe is....
tja, is coke nog zo "leuk" als het belangrijker is dan je huis,je kinderen,gezin???liegen bedriegen en alles op het spel zetten door en voor de coke,en gebruikersvriendjes die je uiteindelijk eraan overhoud als "echt"vrienden??er gaat teveel kapot door die tering zooi!!!!!
Coke is lekker tja, is coke nog zo "leuk" als het belangrijker is dan je huis,je kinderen,gezin???liegen bedriegen en alles op het spel zetten door en voor de coke,en gebruikersvriendjes die je uiteindelijk eraan overhoud als "echt"vrienden??er gaat teveel kapot door die tering zooi!!!!!
je kan ook tever gaan he...
als je echt denkt dat je daaruit kan aflezen wat schadelijker is..
gooi maar eens een plak ham in een glas cola..
Als je meer studies gaat lezen, en je er dus in verdiept..Ja zeker.. Ene een studie die bewijst dat Cola onherselbare hersen schade teweeg breng.....????? Kom maar op...laat zien die url?? hahaha En daar komt nog bij dat de cola via je slokdarm naar de maag gaat, die beide zijn beschermt met een soort beschermlaagje die zuur(in dit geval co2) resistent is.
laatste aanpassing
Ene een studie die bewijst dat Cola onherselbare hersen schade teweeg breng.....????? Kom maar op...laat zien die url??
hallo zeg ik dat dan?? jij noemt zo'n idioot voorbeeld met die biefstukken!
hahaha En daar komt nog bij dat de cola via je slokdarm naar de maag gaat, die beide zijn beschermt met een soort beschermlaagje die zuur(in dit geval co2) resistent is.
met PEP hetzelfde geval..
Al je geld gaat er aan op, klotezooi!!!
met PEP hetzelfde geval..
nee, om dat pep sythetisch is gemaakt van oplosmiddelen...bijt dat alles weg..ook het beschemlaagje(eiwit). En dat jij mijn voorbeeld idioot vind...zegt meer over jou dan over mij of mijn voorbeeld.
hatseeeeeeeeeeee hatseeeeeeeeeeeee
donateur
Als je meer studies gaat lezen, en je er dus in verdiept..Ja zeker.. Ene een studie die bewijst dat Cola onherselbare hersen schade teweeg breng.....????? Kom maar op...laat zien die url??
laat mij maar eens een studie zien die überhaupt aantoont dat er drugs is die onherstelbare schade aan je hersenen toebrengt
die zijn er niet
er is wel aangetoond dat er aanwijzingen zijn die daar op duiden, maar echt aangetoond is het nog niet
niet van pep, coke, wiet etc.
dus ook jij lult uit je nek
hatseeeeeeeeeeehatseeeeeeeeeee
hatseeeeeeeeeee geloof er nix van
laat mij maar eens een studie zien die überhaupt aantoont dat er drugs is die onherstelbare schade aan je hersenen toebrengt
die zijn er niet
er is wel aangetoond dat er aanwijzingen zijn die daar op duiden, maar echt aangetoond is het nog niet
niet van pep, coke, wiet etc.
dus ook jij lult uit je nek
begin jij nou eerst maar eens te leren googelen en/of echt studies te lezen voordat je onzin uikraamt...look at the pic (@ the left) and STFU...
05-04-2006 Zwaar xtc-gebruik wist je geheugen
Source: Het Volk(B)
Pubdate: 5 april 2006
Groot-Brittanië telt het grootste aantal zware xtc-gebruikers in Europa. Dat blijkt uit onderzoek van Britse wetenschappers aan de St.George Medical School in Londen. België en Nederland bungelen onderaan het
lijstje. Veertigduizend xtc-pillen slikken over een periode van negen jaar. Dit ongelukkige record staat op naam van Mr. A, zoals Britse wetenschappers van de St.George Medical School in Londen hun studieobject noemen. Zij onderzochten de 37-jarige gebruiker gedurende vijf maanden.
Uit de studie van de Londense school, eergisteren gepubliceerd in het vakblad British Journal of Psychopharmacology , blijkt dat de Britten de zwaarste xtc-gebruikers zijn in Europa. Zo'n 750.000 partygangers
slikken samen 26 miljoen pillen per jaar. In ons land loopt het niet zo'n vaart. Peer van der Kreeft, hoofd Preventie van het Drughulpcentrum De Sleutel: ,,In België is het aantal zware gebruikers miniem. Net zoals in Nederland, waar onderzoek heeft uitgewezen dat het slechts om een
vierhonderdtal mensen gaat.''
Zwaar xtc-gebruik kan nefaste gevolgen hebben. De onderzoekers van de St. George Medical School lieten weten dat Mr.A leed aan geheugenverlies op korte termijn. ,,Dat bevestigt ook wat eerdere studies hebben
uitgewezen'', meent Anne Van Buyse, psychiater bij De Sleutel. ,,Wie de
partydrug xtc dagelijks gebruikt, loopt onherstelbare hersenschade op."
--
MAP-NL
so again look at the pic ....stfu
laatste aanpassing
Cocaine Dependence And Withdrawal: Neuroadaptive Changes In Brain Reward And Stress Systems
Friedbert Weiss, Ph.D.
The Scripps Research Institute
La Jolla, CA
A growing body of evidence indicates that chronic cocaine administration can produce profound and long-lasting changes in brain neurochemical and neuroendocrine systems. At the behavioral level, evidence is accumulating that chronic use of cocaine compromises the neural mechanisms that mediate positive reinforcement. This is illustrated, for example, by findings that cocaine acutely facilitates the rewarding effects of intracranial self-stimulation, while withdrawal after chronic use leads to an impairment in the rewarding efficacy of electrical brain stimulation (Markou and Koob 1991). Findings such as these have given rise to the view that compulsive drug-seeking behavior associated with cocaine (and other drugs of abuse) may be the result of adaptive processes within the central nervous system that oppose the acute reinforcing actions of drugs, leading both to a "blunting" of mechanisms that mediate positive reinforcement and the emergence of affective changes during withdrawal that may motivate continued use of the drug (for example, anxiety, dysphoria, and depression) during withdrawal (Koob and Bloom 1988; Koob et al. 1993; Wise 1996).
The following discussion reviews both earlier and recent studies that have sought to identify the brain neurochemical processes responsible for the compromised state of the reward system after chronic cocaine abuse and the significance of those processes in the transition from controlled drug use to compulsive drug-taking.
Neuroadaptive Changes Within Brain Reward Circuitries
Intravenous self-administration in rodents has been used successfully to study cocaine-reinforced behavior. This methodology has significantly advanced the understanding of the neurobiological basis of cocaine reinforcement and has established a critical role for the mesoaccumbens dopamine (DA) systems in cocaine's acute reinforcing effects. More recently, studies employing intracranial microdialysis measures of DA in the nucleus accumbens (NAc) of cocaine self-administering rats have confirmed the significance of DA in cocaine reward and extended our understanding of interactions among cocaine, DA, and other transmitters in this brain region in the regulation of cocaine-seeking behavior.
When given the opportunity, both human cocaine abusers and laboratory animals will often self-administer cocaine in sustained episodes that can last from several hours to days. In humans, in particular, this so-called binge pattern of cocaine abuse is associated with severe abstinence syndrome. In animals, termination of access to cocaine after long-term unrestricted intravenous self-administration produces behavioral disruptions and reward deficits believed to be indicative of dependence and withdrawal (Markou and Koob 1991). Therefore, this model was employed in conjunction with intracranial microdialysis to study the neurochemical consequences of long-term cocaine self-administration and cocaine withdrawal.
Dopamine.
Cocaine self-administration produced persistent elevations in extracellular DA concentrations in the NAc that remained stable throughout 12- to 24-hour periods of drug availability. Withdrawal from cocaine resulted in a marked suppression of DA release below basal levels prior to self-administration (Weiss et al. 1992b). Maximal inhibition of DA efflux was reached within 2 to 4 hours postcocaine, and the depression in extracellular DA levels did not recover within a 12-hour monitoring period. The degree of suppression of DA release was positively correlated with the number of hours of continuous cocaine self-administration before withdrawal. Interestingly, as shown in earlier work, deficits in brain stimulation reward also increased as a function of the duration of continuous self-administration prior to withdrawal and were reversible by administration of bromocriptine (Markou and Koob 1991, 1992; Weiss et al. 1995). These data implicate a link between the withdrawal-associated impairment in mesolimbic DA neurotransmission and behavioral abstinence symptoms as measured by attenuated brain stimulation reward. However, it is important to note that brain stimulation reward deficits are already evident shortly after termination of access to cocaine, at a time when there is still some residual elevation, rather than a deficit, in accumbal extracellular DA levels. This observation supports the hypothesis that sustained dopaminergic stimulation by long-term cocaine self-administration leads to adaptation of brain mechanisms that mediate positive reinforcement.
Serotonin.
Cocaine self-administration not only increases extracellular DA levels in the NAc but also produces similar elevations in extracellular serotonin (5-HT). Given the established role of 5-HT in depression, a prominent cocaine withdrawal symptom, it was of interest to determine whether cocaine withdrawal exerts disruptive effects on 5-HT neurotransmission.
Withdrawal after 12 hours of unrestricted access to cocaine produced a substantial suppression of 5-HT release in the NAc. Compared with basal 5-HT levels in cocaine-naive controls, 5-HT efflux as measured by quantitative microdialysis methods decreased by more than 50 percent as early as 6 hours postcocaine (Parsons et al. 1995). In contrast to the serotonergic deficits after long-term cocaine self-administration, only a trend toward suppression of basal 5-HT release was apparent in rats after 24 hours of abstinence from daily 3-hour limited-access self-administration. These findings are consistent with several reports in the literature of supersensitivity of 5-HT1a autoreceptors and increased density of 5-HT uptake sites after intermittent cocaine administration, but they also suggest that marked extracellular consequences of these presynaptic changes become evident only after prolonged periods of continuous cocaine self-administration. Decreased serotonergic transmission has been implicated in symptoms of numerous psychiatric disorders such as depression, panic disorder, insomnia, impulsiveness, and aggression-symptoms also associated with cocaine abstinence. Therefore, the deficit in extracellular 5-HT concentrations may contribute directly to many aspects of the cocaine withdrawal syndrome.
In addition to suppressing the release of 5-HT, withdrawal after long-term access to intravenous cocaine altered the sensitivity of 5-HT1b receptors. Locomotor activation in response to a 5-HT1b agonist (RU 24969) was diminished during the first 2 days of cocaine withdrawal, while a persistent rebound supersensitivity to 5-HT1b receptor activation emerged 1 week after cocaine withdrawal. The initial subsensitivity is likely to reflect an adaptive "downregulation" of 5-HT1b receptors that develops during long-term cocaine self-administration to compensate for the sustained cocaine-induced increases in synaptic 5-HT levels. Conversely, the subsequent supersensitivity is presumably the result of sustained extracellular 5-HT deficiency during cocaine withdrawal. These findings implicate 5-HT1b receptors, both in the cocaine withdrawal syndrome and in locomotor sensitization produced by repeated cocaine administration.
Recent studies have implicated the 5-HT1b receptor in the acute reinforcing actions of cocaine. The 5-HT1b agonists produced a dose-dependent shift to the left in the dose-effect function for self-administered cocaine and elevated breaking points for cocaine on a progressive ratio schedule (Parsons et al., submitted). The enhancement of cocaine reward by 5-HT1b receptor activation appeared to result from an augmentation in the accumulation of extracellular DA in the NAc induced by cocaine, a finding that suggests that 5-HT1b receptors, via stimulation by endogenous 5-HT, may have a role in cocaine reinforcement. The subsensitivity of 5-HT1b receptors during the early withdrawal phase is, therefore, interesting, not only with regard to its role in cocaine withdrawal but also with regard to the general hypothesis that dependence may result from adaptation of central reward mechanisms.
Changes In Brain Stress Systems After Chronic Cocaine
Recently, much attention has been directed at understanding the role of the nonneuroendocrine corticotropin-releasing factor (CRF) system in the central nucleus of the amygdala (CeA) in the affective consequences of stress and in withdrawal from drugs of abuse. The CeA is part of a complex neural circuitry regulating behavioral and autonomic responsiveness to stressful stimuli. In particular, CRF neurons in the CeA are thought to have an essential role in the mediation of emotional responses to stress, such as anxiety. Anxiety and stress-like symptoms are an integral part of drug withdrawal syndromes, raising the possibility that these withdrawal signs may involve activation of CRF neuronal mechanisms in the CeA.
Initial findings indicated that acute intraperitoneal injections of cocaine increase CRF release in the CeA of rats. This effect was significantly enhanced by 2 weeks of daily cocaine pretreatment, implicating CRF mechanisms in the CeA in cocaine sensitization as well as in the cross-sensitization between stress and psychostimulants (Richter et al. 1995). In contrast to the effects of noncontingent, intermittent cocaine administration, however, CRF release in the CeA was significantly suppressed by cocaine in self-administering rats as measured after completion of 2 weeks of cocaine self-administration training. Moreover, in these animals, cocaine withdrawal after 12 hours of continuous access to the drug produced a profound increase in CRF release, which reached peak levels of approximately 400 percent of baseline between 11 and 12 hours postcocaine (Richter and Weiss, submitted).
These data provide support for involvement of CRF mechanisms in the CeA in the motivational effects of cocaine. Central administration of CRF has stress-like anxiogenic and activational consequences in rats that can be effectively reversed by treatments that interfere with CRF transmission in the CeA. The effects of exogenous CRF resemble the behavioral signs of cocaine withdrawal in animals; these effects may be comparable to human withdrawal symptoms such as anxiety, agitation, irritability, restlessness, and confusion. Thus, the activation of CRF release in the CeA during withdrawal may provide a neurochemical basis for aspects of the cocaine abstinence syndrome. In contrast, the suppression of CRF release by cocaine during the self-administration stage may implicate attenuation of CRF release in the CeA as an element in the reinforcing actions of cocaine. Finally, these data extend previous observations on the activation of CRF mechanisms in the CeA during opiate, ethanol, and cannabinoid withdrawal and implicate enhanced amygdaloid CRF release as a common mechanism in symptoms of anxiety and negative affect that are typically associated with drug withdrawal syndromes (de Fonseca et al. 1997; Merlo Pich et al. 1995).
The evidence of a hyperactivity within an important brain stress regulatory center during cocaine withdrawal is intriguing in view of the established role of stress in drug abuse and dependence. Stress is a major determinant of relapse in humans and can increase the intake of psychostimulant drugs; it can also facilitate the acquisition of psychostimulant self-administration in laboratory animals. While many stress-associated drug-seeking behaviors may involve activation of the hypothalamic CRF system and the hypothalamic-pituitary-adrenal axis, the present data support an essential role for amygdalar CRF neurons in drug-seeking behavior motivated by stress or anxiety effects related to cocaine abstinence.
Studies examining the interaction between stress and psychostimulant withdrawal indicate that, in addition to disturbances in the brain CRF system, chronic psychostimulant exposure can disrupt normal stress responses at other levels. For example, not only did termination of daily amphetamine treatment result in a long-lasting deficit in extracellular DA concentrations in the NAc, but also stimulation of DA release in response to restraint stress, which is a typical response to this stressor in drug-naive animals, was no longer observed during amphetamine withdrawal. In fact, restraint stress produced a persistent reduction in extracellular DA concentration below basal levels that were already lowered by withdrawal from chronic amphetamine (Weiss et al., in press). Thus, certain forms of stress may exacerbate the neurochemical consequences of psychostimulant withdrawal by further lowering extracellular DA levels and, thereby, perhaps contribute to the resumption of drug-seeking behavior and increased likelihood of relapse associated with stress. Moreover, the reversal of the dopaminergic response to immobilization stress was not confined to acute abstinence but was still observed at the same magnitude 7 days postamphetamine. This persistent suppression in DA release after stress may reflect a disruption of mechanisms that regulate affective homeostasis, leading to an impairment in the ability to cope with stress or emotional challenges. Such defects may have important implications for emotional states such as depression or helplessness and for vulnerability to relapse over a prolonged abstinence period.
Chronic Cocaine And Behavioral Plasticity
The data discussed above identify perturbations in brain reward and stress systems as an important element in neuroadaptive changes induced by chronic cocaine. Another important factor associated with chronic use of cocaine (and other drugs of abuse) may involve plasticity within brain circuitries that mediate conditioning effects or stimulus-response associations. Indeed, the classical conditioning of cocaine's pharmacological effects with specific drug-associated environmental stimuli is an important aspect of its behavioral actions. Cocaine-associated stimuli can mimic the drug's locomotor-activating effects and control place preference induced by repeated pairing of cocaine injections with a specific environment. The conditioning of cocaine's rewarding actions with environmental stimuli has important implications for its abuse potential. Clinical observations suggest that stimuli previously associated with availability or self-administration of the drug can evoke intense subjective feelings of craving and can trigger episodes of relapse in abstinent cocaine abuse patients.
Experimental studies of drug-seeking behavior associated with drug-related stimuli in rats indicate that incentive motivational stimuli associated with cocaine can elicit and maintain robust cocaine-seeking behavior in the absence of drug availability. For example, rats responding for presentation of conditioned stimuli previously paired with food or cocaine showed a strong shift in preference for a cocaine- over a food-associated stimulus after receiving a noncontingent "priming" injection of cocaine. This effect was particularly sensitive to reversal by a dopamine D1 antagonist, implicating activation of D1 receptors in the motivational effects of cocaine under these conditions.
In rats trained to self-administer cocaine intravenously, presentation of a discriminative stimulus previously predictive of cocaine availability elicited significant and persistent responding after extended periods of abstinence and increased DA efflux in the NAc. The reinstatement of cocaine-seeking behavior was blocked by both dopamine D1 and D2 antagonists. Together, these observations implicate activation of dopaminergic mechanisms in the motivational effects of drug-associated environmental stimuli and drug-priming. Moreover, these data suggest that cocaine-related cues may exert a "priming" action since, like cocaine, these stimuli increase extracellular levels of DA in the NAc.
Summary
It has been proposed that drug addiction is the result of neuroadaptive processes within the central nervous system that oppose the acute reinforcing actions of drugs of abuse (Koob and Bloom 1988), leading to impairment in the mechanisms that mediate positive reinforcement and the emergence of affective changes such as anxiety, dysphoria, and depression during withdrawal. The results reveal perturbations in DA and 5-HT transmission in the NAc-neurochemical systems that are activated by cocaine self-administration and are deficient during withdrawal-as potential substrates for these affective changes. In addition, the results implicate neuroadaptive changes in extrahypothalamic CRF neurons and other brain stress circuitries in the motivational effects of psychostimulant withdrawal. Finally, it appears that environmental cues that become conditioned to the positive reinforcing effects of cocaine can mimic the pharmacological effect of this agent and, thereby, can initiate and maintain cocaine-seeking behavior.
Acknowledgment
This research was supported by National Institute on Drug Abuse Grant No. DA-07348.
References
Rodriguez de Fonseca, F.; Carrera, M.R.A.; Navarro, M.; Koob, G.F.; and Weiss, F. Activation of corticotropin releasing factor in the limbic system during cannabinoid withdrawal. Science 276:2050 -2054, 1997.
Koob, G.F., and Bloom, F.E. Cellular and molecular mechanisms of drug dependence. Science 242:715- 723, 1988.
Koob, G.F.; Markou, A.; Weiss, F.; and Schultei s, G. Opponent process and drug dependence: Neurobiological mechanisms. Semin Neurosci 5:351-35 8, 1993.
Markou, A., and Koob, G.F. Postcocaine anhedonia: An animal model of cocaine withdrawal. Neuropsychopharmacolog y 4:17-26, 1991.
Markou, A., and Koob, G.F. Bromocriptine reverses the elevation in intracranial self-stimulation thresholds observed in a rat model of cocaine withdrawal. Neuropsychopharmacolog y 7:213-22 4, 1992.
Pich, E.M.; Lorang, M.; Yeganeh, M.; Rodriguez de Fonseca, F.; Raber, J.; Koob, G.F.; and Weiss, F. Increase of extracellular corticotropin-releasing factor-like immunoreactivity levels in the amygdala of awake rats during restraint stress and ethanol withdrawal as measured by microdialysis. J Neurosci 15:5439- 5447, 1995.
Parsons, L.H.; Kerr, T.M.; Weiss, F.; and Koob, G.F. Serotonin -1B receptor stimulation enhances cocaine reinforcement: Behavioral and neurochemical studies in rats. J Neurosci, submitted.
Parsons, L.H.; Koob, G.F.; and Weiss, F. Serotonin dysfunction in the nucleus accumbens of rats during withdrawal after unlimited access to intravenous cocaine. J Pharmac ol Exp Ther 274:1182 -1191, 1995.
Richter, R.M.; Pich, E.M.; Koob, G.F.; and Weiss, F. Sensitization of cocaine-stimulated increase in extracellular levels of corticotropin-releasing factor from the rat amygdala after repeated administration as determined by intracranial microdialysis. Neurosci Lett 187:169- 172, 1995.
Richter, R.M., and Weiss, F. In vivo CRF release in rat amygdala is increased during withdrawal after cocaine self-administration with unlimited access. J Neurosci, submitted.
Weiss, F.; Hurd, Y.L.; Ungerstedt, U.; Markou, A.; Plotsky, P.M.; and Koob, G.F. Neurochemical correlates of cocaine and ethanol self-administration . In: The Neurobiology of Drug and Alcohol Addiction. Kalivas, P.W., and Samson, H.H., eds. Ann N Y Acad Sci 654:220- 241, 1992a.
Weiss, F.; Imperato, A.; Casu, M.A.; Mascia, M.S.; and Gessa, G.L. Opposite effects of stress on dopamine release in the limbic system of drug-naive and chronically amphetamine-treated rats. Eur J Pharmacol 337:219- 222, 1997.
Weiss, F.; Markou, A.; Lorang, M.T.; and Koob, G.F. Basal extracellular dopamine levels in the nucleus acumbens are decreased during cocaine withdrawal after unlimited- access self-administration . Brain Res 593:314- 318, 1992b.
Weiss, F.; Parsons, L.H.; and Markou, A. Neurochemistry of cocaine withdrawal. In: The Neurobiology of Cocaine: Cellular and Molecular Mechanisms. Hammer, Jr., R.L., ed. Boca Raton, FL: CRC Press, 1995. pp. 163-180.
Wise, R.A. Neurobiology of addiction. Curr Opin Neurobiol6:243-251, 1996.
NIDA
en zo kan ik er nogwel een paar plaatsen, maar daar heb ik geen zin in, ook gezien die nog wat meer wetenschappelijk geschreven zijn en de meeste hier daar toch geen bal aan vinden...mzzl OUT
Friedbert Weiss, Ph.D.
The Scripps Research Institute
La Jolla, CA
A growing body of evidence indicates that chronic cocaine administration can produce profound and long-lasting changes in brain neurochemical and neuroendocrine systems. At the behavioral level, evidence is accumulating that chronic use of cocaine compromises the neural mechanisms that mediate positive reinforcement. This is illustrated, for example, by findings that cocaine acutely facilitates the rewarding effects of intracranial self-stimulation, while withdrawal after chronic use leads to an impairment in the rewarding efficacy of electrical brain stimulation (Markou and Koob 1991). Findings such as these have given rise to the view that compulsive drug-seeking behavior associated with cocaine (and other drugs of abuse) may be the result of adaptive processes within the central nervous system that oppose the acute reinforcing actions of drugs, leading both to a "blunting" of mechanisms that mediate positive reinforcement and the emergence of affective changes during withdrawal that may motivate continued use of the drug (for example, anxiety, dysphoria, and depression) during withdrawal (Koob and Bloom 1988; Koob et al. 1993; Wise 1996).
The following discussion reviews both earlier and recent studies that have sought to identify the brain neurochemical processes responsible for the compromised state of the reward system after chronic cocaine abuse and the significance of those processes in the transition from controlled drug use to compulsive drug-taking.
Neuroadaptive Changes Within Brain Reward Circuitries
Intravenous self-administration in rodents has been used successfully to study cocaine-reinforced behavior. This methodology has significantly advanced the understanding of the neurobiological basis of cocaine reinforcement and has established a critical role for the mesoaccumbens dopamine (DA) systems in cocaine's acute reinforcing effects. More recently, studies employing intracranial microdialysis measures of DA in the nucleus accumbens (NAc) of cocaine self-administering rats have confirmed the significance of DA in cocaine reward and extended our understanding of interactions among cocaine, DA, and other transmitters in this brain region in the regulation of cocaine-seeking behavior.
When given the opportunity, both human cocaine abusers and laboratory animals will often self-administer cocaine in sustained episodes that can last from several hours to days. In humans, in particular, this so-called binge pattern of cocaine abuse is associated with severe abstinence syndrome. In animals, termination of access to cocaine after long-term unrestricted intravenous self-administration produces behavioral disruptions and reward deficits believed to be indicative of dependence and withdrawal (Markou and Koob 1991). Therefore, this model was employed in conjunction with intracranial microdialysis to study the neurochemical consequences of long-term cocaine self-administration and cocaine withdrawal.
Dopamine.
Cocaine self-administration produced persistent elevations in extracellular DA concentrations in the NAc that remained stable throughout 12- to 24-hour periods of drug availability. Withdrawal from cocaine resulted in a marked suppression of DA release below basal levels prior to self-administration (Weiss et al. 1992b). Maximal inhibition of DA efflux was reached within 2 to 4 hours postcocaine, and the depression in extracellular DA levels did not recover within a 12-hour monitoring period. The degree of suppression of DA release was positively correlated with the number of hours of continuous cocaine self-administration before withdrawal. Interestingly, as shown in earlier work, deficits in brain stimulation reward also increased as a function of the duration of continuous self-administration prior to withdrawal and were reversible by administration of bromocriptine (Markou and Koob 1991, 1992; Weiss et al. 1995). These data implicate a link between the withdrawal-associated impairment in mesolimbic DA neurotransmission and behavioral abstinence symptoms as measured by attenuated brain stimulation reward. However, it is important to note that brain stimulation reward deficits are already evident shortly after termination of access to cocaine, at a time when there is still some residual elevation, rather than a deficit, in accumbal extracellular DA levels. This observation supports the hypothesis that sustained dopaminergic stimulation by long-term cocaine self-administration leads to adaptation of brain mechanisms that mediate positive reinforcement.
Serotonin.
Cocaine self-administration not only increases extracellular DA levels in the NAc but also produces similar elevations in extracellular serotonin (5-HT). Given the established role of 5-HT in depression, a prominent cocaine withdrawal symptom, it was of interest to determine whether cocaine withdrawal exerts disruptive effects on 5-HT neurotransmission.
Withdrawal after 12 hours of unrestricted access to cocaine produced a substantial suppression of 5-HT release in the NAc. Compared with basal 5-HT levels in cocaine-naive controls, 5-HT efflux as measured by quantitative microdialysis methods decreased by more than 50 percent as early as 6 hours postcocaine (Parsons et al. 1995). In contrast to the serotonergic deficits after long-term cocaine self-administration, only a trend toward suppression of basal 5-HT release was apparent in rats after 24 hours of abstinence from daily 3-hour limited-access self-administration. These findings are consistent with several reports in the literature of supersensitivity of 5-HT1a autoreceptors and increased density of 5-HT uptake sites after intermittent cocaine administration, but they also suggest that marked extracellular consequences of these presynaptic changes become evident only after prolonged periods of continuous cocaine self-administration. Decreased serotonergic transmission has been implicated in symptoms of numerous psychiatric disorders such as depression, panic disorder, insomnia, impulsiveness, and aggression-symptoms also associated with cocaine abstinence. Therefore, the deficit in extracellular 5-HT concentrations may contribute directly to many aspects of the cocaine withdrawal syndrome.
In addition to suppressing the release of 5-HT, withdrawal after long-term access to intravenous cocaine altered the sensitivity of 5-HT1b receptors. Locomotor activation in response to a 5-HT1b agonist (RU 24969) was diminished during the first 2 days of cocaine withdrawal, while a persistent rebound supersensitivity to 5-HT1b receptor activation emerged 1 week after cocaine withdrawal. The initial subsensitivity is likely to reflect an adaptive "downregulation" of 5-HT1b receptors that develops during long-term cocaine self-administration to compensate for the sustained cocaine-induced increases in synaptic 5-HT levels. Conversely, the subsequent supersensitivity is presumably the result of sustained extracellular 5-HT deficiency during cocaine withdrawal. These findings implicate 5-HT1b receptors, both in the cocaine withdrawal syndrome and in locomotor sensitization produced by repeated cocaine administration.
Recent studies have implicated the 5-HT1b receptor in the acute reinforcing actions of cocaine. The 5-HT1b agonists produced a dose-dependent shift to the left in the dose-effect function for self-administered cocaine and elevated breaking points for cocaine on a progressive ratio schedule (Parsons et al., submitted). The enhancement of cocaine reward by 5-HT1b receptor activation appeared to result from an augmentation in the accumulation of extracellular DA in the NAc induced by cocaine, a finding that suggests that 5-HT1b receptors, via stimulation by endogenous 5-HT, may have a role in cocaine reinforcement. The subsensitivity of 5-HT1b receptors during the early withdrawal phase is, therefore, interesting, not only with regard to its role in cocaine withdrawal but also with regard to the general hypothesis that dependence may result from adaptation of central reward mechanisms.
Changes In Brain Stress Systems After Chronic Cocaine
Recently, much attention has been directed at understanding the role of the nonneuroendocrine corticotropin-releasing factor (CRF) system in the central nucleus of the amygdala (CeA) in the affective consequences of stress and in withdrawal from drugs of abuse. The CeA is part of a complex neural circuitry regulating behavioral and autonomic responsiveness to stressful stimuli. In particular, CRF neurons in the CeA are thought to have an essential role in the mediation of emotional responses to stress, such as anxiety. Anxiety and stress-like symptoms are an integral part of drug withdrawal syndromes, raising the possibility that these withdrawal signs may involve activation of CRF neuronal mechanisms in the CeA.
Initial findings indicated that acute intraperitoneal injections of cocaine increase CRF release in the CeA of rats. This effect was significantly enhanced by 2 weeks of daily cocaine pretreatment, implicating CRF mechanisms in the CeA in cocaine sensitization as well as in the cross-sensitization between stress and psychostimulants (Richter et al. 1995). In contrast to the effects of noncontingent, intermittent cocaine administration, however, CRF release in the CeA was significantly suppressed by cocaine in self-administering rats as measured after completion of 2 weeks of cocaine self-administration training. Moreover, in these animals, cocaine withdrawal after 12 hours of continuous access to the drug produced a profound increase in CRF release, which reached peak levels of approximately 400 percent of baseline between 11 and 12 hours postcocaine (Richter and Weiss, submitted).
These data provide support for involvement of CRF mechanisms in the CeA in the motivational effects of cocaine. Central administration of CRF has stress-like anxiogenic and activational consequences in rats that can be effectively reversed by treatments that interfere with CRF transmission in the CeA. The effects of exogenous CRF resemble the behavioral signs of cocaine withdrawal in animals; these effects may be comparable to human withdrawal symptoms such as anxiety, agitation, irritability, restlessness, and confusion. Thus, the activation of CRF release in the CeA during withdrawal may provide a neurochemical basis for aspects of the cocaine abstinence syndrome. In contrast, the suppression of CRF release by cocaine during the self-administration stage may implicate attenuation of CRF release in the CeA as an element in the reinforcing actions of cocaine. Finally, these data extend previous observations on the activation of CRF mechanisms in the CeA during opiate, ethanol, and cannabinoid withdrawal and implicate enhanced amygdaloid CRF release as a common mechanism in symptoms of anxiety and negative affect that are typically associated with drug withdrawal syndromes (de Fonseca et al. 1997; Merlo Pich et al. 1995).
The evidence of a hyperactivity within an important brain stress regulatory center during cocaine withdrawal is intriguing in view of the established role of stress in drug abuse and dependence. Stress is a major determinant of relapse in humans and can increase the intake of psychostimulant drugs; it can also facilitate the acquisition of psychostimulant self-administration in laboratory animals. While many stress-associated drug-seeking behaviors may involve activation of the hypothalamic CRF system and the hypothalamic-pituitary-adrenal axis, the present data support an essential role for amygdalar CRF neurons in drug-seeking behavior motivated by stress or anxiety effects related to cocaine abstinence.
Studies examining the interaction between stress and psychostimulant withdrawal indicate that, in addition to disturbances in the brain CRF system, chronic psychostimulant exposure can disrupt normal stress responses at other levels. For example, not only did termination of daily amphetamine treatment result in a long-lasting deficit in extracellular DA concentrations in the NAc, but also stimulation of DA release in response to restraint stress, which is a typical response to this stressor in drug-naive animals, was no longer observed during amphetamine withdrawal. In fact, restraint stress produced a persistent reduction in extracellular DA concentration below basal levels that were already lowered by withdrawal from chronic amphetamine (Weiss et al., in press). Thus, certain forms of stress may exacerbate the neurochemical consequences of psychostimulant withdrawal by further lowering extracellular DA levels and, thereby, perhaps contribute to the resumption of drug-seeking behavior and increased likelihood of relapse associated with stress. Moreover, the reversal of the dopaminergic response to immobilization stress was not confined to acute abstinence but was still observed at the same magnitude 7 days postamphetamine. This persistent suppression in DA release after stress may reflect a disruption of mechanisms that regulate affective homeostasis, leading to an impairment in the ability to cope with stress or emotional challenges. Such defects may have important implications for emotional states such as depression or helplessness and for vulnerability to relapse over a prolonged abstinence period.
Chronic Cocaine And Behavioral Plasticity
The data discussed above identify perturbations in brain reward and stress systems as an important element in neuroadaptive changes induced by chronic cocaine. Another important factor associated with chronic use of cocaine (and other drugs of abuse) may involve plasticity within brain circuitries that mediate conditioning effects or stimulus-response associations. Indeed, the classical conditioning of cocaine's pharmacological effects with specific drug-associated environmental stimuli is an important aspect of its behavioral actions. Cocaine-associated stimuli can mimic the drug's locomotor-activating effects and control place preference induced by repeated pairing of cocaine injections with a specific environment. The conditioning of cocaine's rewarding actions with environmental stimuli has important implications for its abuse potential. Clinical observations suggest that stimuli previously associated with availability or self-administration of the drug can evoke intense subjective feelings of craving and can trigger episodes of relapse in abstinent cocaine abuse patients.
Experimental studies of drug-seeking behavior associated with drug-related stimuli in rats indicate that incentive motivational stimuli associated with cocaine can elicit and maintain robust cocaine-seeking behavior in the absence of drug availability. For example, rats responding for presentation of conditioned stimuli previously paired with food or cocaine showed a strong shift in preference for a cocaine- over a food-associated stimulus after receiving a noncontingent "priming" injection of cocaine. This effect was particularly sensitive to reversal by a dopamine D1 antagonist, implicating activation of D1 receptors in the motivational effects of cocaine under these conditions.
In rats trained to self-administer cocaine intravenously, presentation of a discriminative stimulus previously predictive of cocaine availability elicited significant and persistent responding after extended periods of abstinence and increased DA efflux in the NAc. The reinstatement of cocaine-seeking behavior was blocked by both dopamine D1 and D2 antagonists. Together, these observations implicate activation of dopaminergic mechanisms in the motivational effects of drug-associated environmental stimuli and drug-priming. Moreover, these data suggest that cocaine-related cues may exert a "priming" action since, like cocaine, these stimuli increase extracellular levels of DA in the NAc.
Summary
It has been proposed that drug addiction is the result of neuroadaptive processes within the central nervous system that oppose the acute reinforcing actions of drugs of abuse (Koob and Bloom 1988), leading to impairment in the mechanisms that mediate positive reinforcement and the emergence of affective changes such as anxiety, dysphoria, and depression during withdrawal. The results reveal perturbations in DA and 5-HT transmission in the NAc-neurochemical systems that are activated by cocaine self-administration and are deficient during withdrawal-as potential substrates for these affective changes. In addition, the results implicate neuroadaptive changes in extrahypothalamic CRF neurons and other brain stress circuitries in the motivational effects of psychostimulant withdrawal. Finally, it appears that environmental cues that become conditioned to the positive reinforcing effects of cocaine can mimic the pharmacological effect of this agent and, thereby, can initiate and maintain cocaine-seeking behavior.
Acknowledgment
This research was supported by National Institute on Drug Abuse Grant No. DA-07348.
References
Rodriguez de Fonseca, F.; Carrera, M.R.A.; Navarro, M.; Koob, G.F.; and Weiss, F. Activation of corticotropin releasing factor in the limbic system during cannabinoid withdrawal. Science 276:2050 -2054, 1997.
Koob, G.F., and Bloom, F.E. Cellular and molecular mechanisms of drug dependence. Science 242:715- 723, 1988.
Koob, G.F.; Markou, A.; Weiss, F.; and Schultei s, G. Opponent process and drug dependence: Neurobiological mechanisms. Semin Neurosci 5:351-35 8, 1993.
Markou, A., and Koob, G.F. Postcocaine anhedonia: An animal model of cocaine withdrawal. Neuropsychopharmacolog y 4:17-26, 1991.
Markou, A., and Koob, G.F. Bromocriptine reverses the elevation in intracranial self-stimulation thresholds observed in a rat model of cocaine withdrawal. Neuropsychopharmacolog y 7:213-22 4, 1992.
Pich, E.M.; Lorang, M.; Yeganeh, M.; Rodriguez de Fonseca, F.; Raber, J.; Koob, G.F.; and Weiss, F. Increase of extracellular corticotropin-releasing factor-like immunoreactivity levels in the amygdala of awake rats during restraint stress and ethanol withdrawal as measured by microdialysis. J Neurosci 15:5439- 5447, 1995.
Parsons, L.H.; Kerr, T.M.; Weiss, F.; and Koob, G.F. Serotonin -1B receptor stimulation enhances cocaine reinforcement: Behavioral and neurochemical studies in rats. J Neurosci, submitted.
Parsons, L.H.; Koob, G.F.; and Weiss, F. Serotonin dysfunction in the nucleus accumbens of rats during withdrawal after unlimited access to intravenous cocaine. J Pharmac ol Exp Ther 274:1182 -1191, 1995.
Richter, R.M.; Pich, E.M.; Koob, G.F.; and Weiss, F. Sensitization of cocaine-stimulated increase in extracellular levels of corticotropin-releasing factor from the rat amygdala after repeated administration as determined by intracranial microdialysis. Neurosci Lett 187:169- 172, 1995.
Richter, R.M., and Weiss, F. In vivo CRF release in rat amygdala is increased during withdrawal after cocaine self-administration with unlimited access. J Neurosci, submitted.
Weiss, F.; Hurd, Y.L.; Ungerstedt, U.; Markou, A.; Plotsky, P.M.; and Koob, G.F. Neurochemical correlates of cocaine and ethanol self-administration . In: The Neurobiology of Drug and Alcohol Addiction. Kalivas, P.W., and Samson, H.H., eds. Ann N Y Acad Sci 654:220- 241, 1992a.
Weiss, F.; Imperato, A.; Casu, M.A.; Mascia, M.S.; and Gessa, G.L. Opposite effects of stress on dopamine release in the limbic system of drug-naive and chronically amphetamine-treated rats. Eur J Pharmacol 337:219- 222, 1997.
Weiss, F.; Markou, A.; Lorang, M.T.; and Koob, G.F. Basal extracellular dopamine levels in the nucleus acumbens are decreased during cocaine withdrawal after unlimited- access self-administration . Brain Res 593:314- 318, 1992b.
Weiss, F.; Parsons, L.H.; and Markou, A. Neurochemistry of cocaine withdrawal. In: The Neurobiology of Cocaine: Cellular and Molecular Mechanisms. Hammer, Jr., R.L., ed. Boca Raton, FL: CRC Press, 1995. pp. 163-180.
Wise, R.A. Neurobiology of addiction. Curr Opin Neurobiol6:243-251, 1996.
NIDA
en zo kan ik er nogwel een paar plaatsen, maar daar heb ik geen zin in, ook gezien die nog wat meer wetenschappelijk geschreven zijn en de meeste hier daar toch geen bal aan vinden...mzzl OUT
Er wordt wel eens beweerd, dat een groot deel van de Westerse literatuur niet zou geschreven zijn als er geen tabak, koffie, wijn of andere stimulantia waren geweest. Een flink deel van onze geschriften en kunst zijn inderdaad tot stand gekomen onder invloed van cocaïne, hennep of opium. In China was de opiumhandel de aanleiding tot twee oorlogen met verstrekkende politieke en historische gevolgen.
Tjah....
Tjah....
laatste aanpassing
wil je over een jaartje wel zien hahahahahahahahaaahahhaahahahahahahahahahahaaaaaaaaaaaa
niet lullig bedoelt maar denk ff aan het leven dat jevroeger had en het leven dat je nu hebt...
god wat baal je dan
niet lullig bedoelt maar denk ff aan het leven dat jevroeger had en het leven dat je nu hebt...
god wat baal je dan
lijkt mij niet dat dat voor mij was bedoelt, gezien mijn leven inverhouding met vroeger zeker is verbeterd
dan nog voor de eigenwijze mensen>>> http://search.atomz.com/search/?sp-q=meth&sp-a=sp10017ea1&sp-advanced=1&sp-p=any&sp-w-control=1&sp-w=alike&sp-d=custom&sp-date-range=-1&sp-start-month=0&sp-start-day=0&sp-start-year=&sp-end-month=0&sp-end-day=0&sp-end-year=&sp-x=any&sp-c=10&sp-m=1&sp-s=0
en http://search.atomz.com/search/?sp-q=amfetamin&sp-a=sp10017ea1&sp-f=iso-8859-1&sp-advanced=1&sp-p=any&sp-w-control=1&sp-w=alike&sp-d=custom&sp-date-range=-1&sp-start-month=0&sp-start-day=0&sp-start-year=&sp-end-month=0&sp-end-day=0&sp-end-year=&sp-x=any&sp-c=10&sp-m=1&sp-s=0
en dan nog een afsluitertje
* Patients with amphetamine intoxication often are identified by a change of mental status alone or associated with another injury and/or illness.
* Central nervous system
o Change of mental status, disorientation, and headache
o Dyskinesias
o Agitation
o Formication
o Symptoms of stroke
* Cardiovascular
o Chest pain
o Palpitations
* Gastrointestinal
o Dry mouth
o Nausea and vomiting
o Diarrhea
* Genitourinary (GU) - Difficult micturition
* Skin/cutaneous
o Diaphoresis
o Erythematous painful rashes, needle marks
o Infected deep ulcerations (ecthyma)
* Ocular - Mydriasis
Physical: Physical examination findings may demonstrate the strong central nervous system and peripheral nervous system stimulation produced by amphetamine compounds. Modification of the basic amphetamine molecule produces compounds with variable effects on target organs. Methamphetamine produces prominent central nervous system effects with minimal cardiovascular stimulation.
Individuals who chronically use amphetamines intravenously are at risk of infection and vascular injury.
* General
o Weight loss
o Hyperactivity, confusion, and agitation (may combine to produce severe hyperthermia, which can be worse in physically restrained individuals)
o Diaphoresis
o Mydriasis
o Anorexia
* Cardiovascular
o Alpha- and beta-adrenergic stimulation can lead to systolic and diastolic blood pressure increases.
o Heart rate may be unchanged or slow in response to hypertension.
o Increasing doses produce tachycardia and other dysrhythmias, including ventricular tachycardia and fibrillation.
o Hypertensive crisis or vasospasm may lead to stroke.
* Respiratory - Persons who smoke amphetamines can develop respiratory distress secondary to pulmonary edema.
* Central nervous system
o Increased alertness
o Euphoria
o Confusion or agitation
o Bruxism
o Stroke caused by acute amphetamine toxicity
* Cutaneous
o Skin flushing
o Infected deep ulcerations (ecthyma) in patients with formication
o Skin track marks, cellulitis, abscesses, phlebitis, or vasculitis with IV use
* Gastrointestinal - Nausea or vomiting
veel lees plezier..mzzl
dan nog voor de eigenwijze mensen>>> http://search.atomz.com/search/?sp-q=meth&sp-a=sp10017ea1&sp-advanced=1&sp-p=any&sp-w-control=1&sp-w=alike&sp-d=custom&sp-date-range=-1&sp-start-month=0&sp-start-day=0&sp-start-year=&sp-end-month=0&sp-end-day=0&sp-end-year=&sp-x=any&sp-c=10&sp-m=1&sp-s=0
en http://search.atomz.com/search/?sp-q=amfetamin&sp-a=sp10017ea1&sp-f=iso-8859-1&sp-advanced=1&sp-p=any&sp-w-control=1&sp-w=alike&sp-d=custom&sp-date-range=-1&sp-start-month=0&sp-start-day=0&sp-start-year=&sp-end-month=0&sp-end-day=0&sp-end-year=&sp-x=any&sp-c=10&sp-m=1&sp-s=0
en dan nog een afsluitertje
* Patients with amphetamine intoxication often are identified by a change of mental status alone or associated with another injury and/or illness.
* Central nervous system
o Change of mental status, disorientation, and headache
o Dyskinesias
o Agitation
o Formication
o Symptoms of stroke
* Cardiovascular
o Chest pain
o Palpitations
* Gastrointestinal
o Dry mouth
o Nausea and vomiting
o Diarrhea
* Genitourinary (GU) - Difficult micturition
* Skin/cutaneous
o Diaphoresis
o Erythematous painful rashes, needle marks
o Infected deep ulcerations (ecthyma)
* Ocular - Mydriasis
Physical: Physical examination findings may demonstrate the strong central nervous system and peripheral nervous system stimulation produced by amphetamine compounds. Modification of the basic amphetamine molecule produces compounds with variable effects on target organs. Methamphetamine produces prominent central nervous system effects with minimal cardiovascular stimulation.
Individuals who chronically use amphetamines intravenously are at risk of infection and vascular injury.
* General
o Weight loss
o Hyperactivity, confusion, and agitation (may combine to produce severe hyperthermia, which can be worse in physically restrained individuals)
o Diaphoresis
o Mydriasis
o Anorexia
* Cardiovascular
o Alpha- and beta-adrenergic stimulation can lead to systolic and diastolic blood pressure increases.
o Heart rate may be unchanged or slow in response to hypertension.
o Increasing doses produce tachycardia and other dysrhythmias, including ventricular tachycardia and fibrillation.
o Hypertensive crisis or vasospasm may lead to stroke.
* Respiratory - Persons who smoke amphetamines can develop respiratory distress secondary to pulmonary edema.
* Central nervous system
o Increased alertness
o Euphoria
o Confusion or agitation
o Bruxism
o Stroke caused by acute amphetamine toxicity
* Cutaneous
o Skin flushing
o Infected deep ulcerations (ecthyma) in patients with formication
o Skin track marks, cellulitis, abscesses, phlebitis, or vasculitis with IV use
* Gastrointestinal - Nausea or vomiting
veel lees plezier..mzzl
laatste aanpassing
ja maar dat mooie is er wel zo af! probeer eens hero dat schijnt nog veel vetter te zijn!
hatseeeeeeeeeeee
donateur
niet alleen met coke, maar ook met pillen/mdma, pep, efedra enz enz enz
wat is het leven toch mooi met SPEED 