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PubMed2000

Intravenous self-administration of methamphetamine-heroin (speedball) combinations under a progressive-ratio schedule of reinforcement in rats.

The i.v. self-administration by rats of a polydrug combination of methamphetamine and heroin was explored. The rewarding efficacy of a range of methamphetamine doses (0.0625-2.0 mg/kg/injection) alone or in combination with heroin (12.5 microg/kg/injection) was compared using a progressive-ratio (PR) schedule of reinforcement. Breaking points (BP) for one group of rats were determined at each dose of methamphetamine-alone and for another group at each of the same methamphetamine doses plus the heroin dose. The methamphetamine-heroin combination was associated with higher BPs than methamphetamine alone at all doses of methamphetamine. These data demonstrate that methamphetamine-heroin combinations (speedballs) produce a greater rewarding effect than the identical doses of methamphetamine alone and suggest that enhanced reward may underlie the popularity of speedball abuse.

Animals↗

PubMed1997

Generalization of D-, L- and DL-chlorpheniramine and zolantidine to the discriminative stimulus effects of cocaine and methamphetamine.

We recently demonstrated that some H-antagonists have cocaine or methamphetamine-like discriminative stimulus effects. In the present study, the effects of optical isomers of chlorpheniramine (D-, L- and DL-forms) on the discriminative stimulus effects of cocaine and methamphetamine were examined in rats trained to discriminate between cocaine (10.0 mg/kg) or methamphetamine (1.0 mg/kg) and saline, to determine whether these effects of H1-antagonists are mediated by the blockade of H-receptors. In generalization tests with optical isomers of chlorpheniramine, the D-, L- and DL-forms all completely generalized to the discriminative stimulus effects of cocaine, but did not generalize to those of methamphetamine. Dose-generalization by the optical isomers of chlorpheniramine to the discriminative stimulus effects of cocaine did not correlate with the H-antagonistic potency of these drugs. These results suggest that all of the optical isomers of chlorpheniramine have cocaine-like discriminative stimulus effects, but that these effects are not mediated by H1-receptor blockade. On the other hand, the H2-antagonist, zolantidine, generalized to the discriminative stimulus effects of methamphetamine, but not to those of cocaine, suggesting that zolantidine may have methamphetamine-like discriminative stimulus effects. In the present study, GBR12909 (dopamine uptake inhibitor) completely generalized to the discriminative stimulus effects of cocaine, but not to those of methamphetamine, whereas apomorphine (dopamine receptor agonist) generalized more potently to the discriminative stimulus effects of methamphetamine than to those of cocaine. These findings imply that although the dopaminergic system plays an important role in the discriminative stimulus effects of both cocaine and methamphetamine, there may be differences between their effects.

Animals↗

PubMed1996

Age-dependent induction and maintenance of sensitization to methamphetamine-induced hyperactivity in mice.

Repeated administrations of methamphetamine (2 mg/kg, s.c.), 10 times at 3-day intervals, induced ambulatory sensitization in all groups of mice that were 13-, 15-, 19-, 23- and 36-week-old at the start of methamphetamine administration. The most prominent sensitization was observed in the 19-week-old mice. Among five groups of mice, even though the mice of 36 weeks old showed the highest sensitivity to methamphetamine at the first administration, they exhibited the lowest sensitization during the latter stage of repeated methamphetamine administration. Methamphetamine sensitization once established was well reproduced by the post-sensitization period of 8 weeks. Furthermore, the group of mice given methamphetamine with post-sensitization interval of 8 weeks (19-week-old mice) exhibited further enhancement of the sensitization. In contrast, the groups of mice given methamphetamine with post-sensitization intervals of 12 and 25 weeks (the 23- and 36-week-old, respectively) showed a significant reduced sensitization, and the latter group failed to reach the level of sensitization previously established. These results suggest that the induction of and maintenance of methamphetamine sensitization are dependent on the age of the mice, and that methamphetamine sensitization once established completely persists for up to 8 weeks.

Age Factors↗

PubMed2006

Prevalence and profile of methamphetamine users in adolescents at a juvenile classification home.

The objective of the present study was to investigate the prevalence and risk factors of methamphetamine use in adolescents at a juvenile classification home. The present subjects were 1362 adolescents (1172 male and 190 female) who had been admitted to the Nagoya Juvenile Classification Home. The participants were divided into two groups, a methamphetamine user group and a control group, based on history of methamphetamine use. The presence of methamphetamine use was analyzed in terms of gender, age, number of admissions, violence (types of crime), history of psychiatric treatment, family history (crime, drug misuse and/or alcohol-related disorder), and experience of being abused by their parents or by the persons who were responsible for raising them. The prevalence of methamphetamine use was 6.8% (93/1362). Multivariate logistic regression analyses indicated that gender (female; odds ratio [OR]: 8.1; 95% confidence interval [CI]: 4.6-14.3), age (OR: 1.8, 95%CI: 1.5-2.1), number of admissions (>2, OR: 2.9, 95%CI: 1.8-4.8), violence (OR: 0.4, 95%CI: 0.2-0.7), history of psychiatric treatment (OR: 8.7, 95%CI: 4.0-19.0), and family history of drug misuse (OR: 4.0, 95%CI: 1.6-9.6) were all significantly associated with methamphetamine use. Approximately 7% of participants used methamphetamine. Female gender was a risk factor. Higher age and multiple admissions suggest the persistency and repetition of delinquency. Methamphetamine users were less violent than control subjects. Psychosocial environment (family history of drug misuse) and psychiatric problems (history of psychiatric treatment) were also related to methamphetamine use.

Adolescent↗

PubMed1993

Striatal dopamine release in vivo following neurotoxic doses of methamphetamine and effect of the neuroprotective drugs, chlormethiazole and dizocilpine.

1. Administration to rats of methamphetamine (15 mg kg-1, i.p.) every 2 h to a total of 4 doses resulted in a neurotoxic loss of striatal dopamine of 36% and of 5-hydroxytryptamine (5-HT) in the cortex (43%) and hippocampus (47%) 3 days later. 2. Administration of chlormethiazole (50 mg kg-1, i.p.) 15 min before each dose of methamphetamine provided complete protection against the neurotoxic loss of monoamines while administration of dizocilpine (1 mg kg-1, i.p.) using the same dose schedule provided substantial protection. 3. Measurement of dopamine release in the striatum by in vivo microdialysis revealed that methamphetamine produced an approximate 7000% increase in dopamine release after the first injection. The enhanced release response was somewhat diminished after the third injection but still around 4000% above baseline. Dizocilpine (1 mg kg-1, i.p.) did not alter this response but chlormethiazole (50 mg kg-1, i.p.) attenuated the methamphetamine-induced release by approximately 40%. 4. Dizocilpine pretreatment did not influence the decrease in the dialysate concentration of the dopamine metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) produced by administration of methamphetamine while chlormethiazole pretreatment decreased the dialysate concentration of these metabolites still further. 5. The concentration of dopamine in the dialysate during basal conditions increased modestly during the course of the experiment. This increase did not occur in chlormethiazole-treated rats. HVA concentrations were unaltered by chlormethiazole administration. 6. Chlormethiazole (100-1000 microM) did not alter methamphetamine (100 microM) or K+ (35 mM)-evoked release of endogenous dopamine from striatal prisms in vitro. 7. Several NMDA antagonists prevent methamphetamine-induced neurotoxicity; however chlormethiazole is not an NMDA antagonist. Inhibition of striatal dopamine function prevents methamphetamine-induced toxicity of both dopamine and 5-HT pathways. Therefore the attenuation of the enhanced dopamine release which occurs in animals given chlormethiazole may be associated with the protective action of this drug against methamphetamine-induced neurotoxicity.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2004

Methamphetamine neurotoxicity in dopamine nerve endings of the striatum is associated with microglial activation.

Methamphetamine intoxication causes long-lasting damage to dopamine nerve endings in the striatum. The mechanisms underlying this neurotoxicity are not known but oxidative stress has been implicated. Microglia are the major antigen-presenting cells in brain and when activated, they secrete an array of factors that cause neuronal damage. Surprisingly, very little work has been directed at the study of microglial activation as part of the methamphetamine neurotoxic cascade. We report here that methamphetamine activates microglia in a dose-related manner and along a time course that is coincident with dopamine nerve ending damage. Prevention of methamphetamine toxicity by maintaining treated mice at low ambient temperature prevents drug-induced microglial activation. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which damages dopamine nerve endings and cell bodies, causes extensive microglial activation in striatum as well as in the substantia nigra. In contrast, methamphetamine causes neither microglial activation in the substantia nigra nor dopamine cell body damage. Dopamine transporter antagonists (cocaine, WIN 35,428 [(-)-2-beta-carbomethoxy-3-beta-(4-fluorophenyl)tropane 1,5-naphthalenedisulfonate], and nomifensine), selective D1 (SKF 82958 [(+/-)-6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide]), D2 (quinpirole), or mixed D1/D2 receptor agonists (apomorphine) do not mimic the effect of methamphetamine on microglia. Hyperthermia, a prominent and dangerous clinical response to methamphetamine intoxication, was also ruled out as the cause of microglial activation. Together, these data suggest that microglial activation represents an early step in methamphetamine-induced neurotoxicity. Other neurochemical effects resulting from methamphetamine-induced overflow of DA into the synapse, but which are not neurotoxic, do not play a role in this response.

Animals↗

PubMed1992

Methamphetamine detection from meconium and amniotic fluid in guinea pigs depends on gestational age and metabolism.

Significant adverse perinatal effects of maternal methamphetamine use have been reported, but little is known about factors influencing methamphetamine screening test results during the perinatal period. We tested the hypothesis that gestational age would affect quantitative recovery of methamphetamine in meconium and amniotic fluid. Time-bred guinea pigs received an intraperitoneal (i.p.) injection of 1 mg/kg methamphetamine at either 44 days (0.65 of term, n = 5), 50 days (0.74, n = 8), 56 days (0.82, n = 9) or 63 days (0.93, n = 4) gestation. At 1 or 7 days after i.p. methamphetamine, meconium and amniotic fluid were collected for quantitative methamphetamine assay by gas chromatography-mass spectrometry. Recovery from amniotic fluid and meconium 1 day after injection was influenced by gestational age. Greater values in amniotic fluid and meconium and a higher percentage of positive samples were seen in older fetuses. Collectively at all gestational ages, combined testing of amniotic fluid and meconium yielded detectable methamphetamine or its metabolites in 87% of guinea pigs 1 day after injection. However, methamphetamine was not detectable 1 week after injection in any sample (n = 63) at either 0.74 or 0.82 of term except for one positive amniotic fluid sample. Finally, demethylation of methamphetamine to amphetamine was higher in older fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗

PubMed2004

Partial recovery of brain metabolism in methamphetamine abusers after protracted abstinence.

OBJECTIVE: Methamphetamine is a highly addictive drug of abuse that is neurotoxic to dopamine terminals. The authors recently reported that decreases in dopamine transporters (used as markers of dopamine terminals) in the striatum of methamphetamine abusers recover with protracted abstinence and that relative to comparison subjects, recently detoxified methamphetamine abusers have lower metabolism in the striatum and thalamus. In this study, the authors assessed whether metabolism recovers with protracted abstinence. METHOD: Brain glucose metabolism was measured with positron emission tomography and [18F]fluorodeoxyglucose in five methamphetamine abusers who were evaluated after both a short (<6 months) and protracted (12-17 months) abstinence interval, eight methamphetamine abusers tested only after protracted abstinence, and 11 comparison subjects who were not drug users. RESULTS: Significantly greater thalamic, but not striatal, metabolism was seen following protracted abstinence relative to metabolism assessed after a short abstinence interval, and this increase was associated with improved performance in motor and verbal memory tests. Relative to the comparison subjects, the methamphetamine abusers tested after protracted abstinence had lower metabolism in the striatum (most accentuated in the caudate and nucleus accumbens) but not in the thalamus. CONCLUSIONS: The persistent decreases in striatal metabolism in methamphetamine abusers could reflect long-lasting changes in dopamine cell activity, and decreases in the nucleus accumbens could account for the persistence of amotivation and anhedonia in detoxified methamphetamine abusers. The recovery of thalamic metabolism could reflect adaptation responses to compensate for the dopamine deficits, and the associated improvement in neuropsychological performance further indicates its functional significance. These results suggest that while protracted abstinence may reverse some of the methamphetamine-induced alterations in brain function, other deficits persist.

Adaptation, Physiological↗

PubMed2004

Effects of neonatal exposure to methamphetamine: catecholamine levels in brain areas of the developing rat.

Neonatal exposure to moderate doses of methamphetamine during the first month of life in the rat affects tyrosine hydroxylase gene expression in the substantia nigra and nigrostriatal tyrosine hydroxylase activity. The main goal of this work was to evaluate the ontogeny of the neurochemical effects of repeated exposure to moderate doses of methamphetamine during the first month of life in the rat. Norepinephrine, dopamine, and dihydroxyphenylacetic acid levels were measured in target areas of methamphetamine: the substantia nigra, ventral tegmental area, caudate-putamen, nucleus accumbens, and medial prefrontal cortex. On postnatal day 1 (PND1), Wistar rat litters, culled to eight pups, sex balanced, were randomly attributed to either methamphetamine or control groups. Methamphetamine groups were administered 10 mg of (+/-)-methamphetamine/kg body weight/day, subcutaneously, from PND1 until the day prior to sacrifice; control groups received isovolumetric saline. Groups were sacrificed on PND7, PND14, and PND30. Neonatal methamphetamine exposure increased norepinephrine levels in the substantia nigra of PND30 rats; on PND14, this variation was evident only in male pups. In the substantia nigra, the dihydroxyphenylacetic/dopamine ratio was also affected in PND30 males. In the ventral tegmental area, catecholamine levels were not affected by methamphetamine. Norepinephrine levels were also increased in the caudate-putamen of PND7 male and PND14 female methamphetamine-exposed pups and in the nucleus accumbens of PND14 female and PND30 male and female pups. Catecholamine levels in the medial prefrontal cortex were not affected by neonatal methamphetamine administration.

Animals↗

PubMed1993

Production and characterization of monoclonal antibody that simultaneously recognizes methamphetamine and its major metabolite.

A series of monoclonal antibodies (mAbs) that react with methamphetamine-bovine serum albumin (MA-BSA) were established by intrasplenic immunization method. Among established 36 clones, two typical mAbs, designated NK-1 and NK-2, were described. The inhibition assay of enzyme-linked immunosorbent assay (ELISA) analysis using methamphetamine analogs indicated that NK-1 showed considerable reactivity not only MA-BSA but also methamphetamine and its major metabolite, para-hydroxymethamphetamine (p-hydroxymethamphetamine). The cross-reactivity between NK-1 and the methamphetamine analogs with modified alkyl side chain, indicates that methyl groups of R5 and R7 in the methamphetamine molecules are important for the maximum affinity. The length of alkyl side chain on methamphetamine significantly affected the binding affinity of NK-1. The results may suggest that NK-1 will recognize not only methamphetamine but also the bridge part of the methamphetamine that binds the methamphetamine molecules to a carrier protein.

Animals↗

PubMed1983

Enzyme immunoassay for methamphetamine.

A competitive enzyme immunoassay for methamphetamine with alkaline phosphatase labeled methamphetamine, Sepharose-antibody and p-nitrophenylphosphate as substrate was developed. The anti-methamphetamine antisera produced in rabbits by immunization with N-(4-aminobutyl) methamphetamine-BSA conjugate were specific for methamphetamine and showed low cross-reactivities with p-OH methamphetamine and amphetamine (metabolites of methamphetamine). The range of methamphetamine measurable by the enzyme immunoassay was 1 to 300 ng/tube. According to the assay, methamphetamine could be detected from urine and extract of hair.

Alkaline Phosphatase↗

PubMed2005

Underlying mechanism of combined effect of methamphetamine and morphine on lethality in mice and therapeutic potential of cooling.

An increase in polydrug abuse is a major problem worldwide. A previous study showed that coadministration of methamphetamine and morphine induced lethality in rodents and humans. However, the underlying mechanisms by which the lethality is increased by the coadministration of methamphetamine and morphine have not been fully understood. Therefore, the present study was designed to determine the mechanism of increased lethality induced by methamphetamine and morphine. Coadministered methamphetamine and morphine increased the lethality by more than 70% in BALB/c mice. Pretreatment with NMDA-receptor antagonists, such as MK-801 and 3-((R)-2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP), and benzamide [poly(ADP-ribose) polymerase (PARP) inhibitor] significantly attenuated the increased lethality induced by methamphetamine and morphine. Furthermore, the lethal effect induced by methamphetamine and morphine was completely attenuated by immediate cooling after the coadministration of methamphetamine and morphine. It has been reported that methamphetamine-induced neurotoxicity can be blocked by lowering the temperature, and this effect might be mediated by a reduction of release of free radicals. These results suggest that activation of NMDA receptors and PARP play an important role in the increased lethality induced by methamphetamine and morphine.

Animals↗

PubMed2006

The infant development, environment, and lifestyle study: effects of prenatal methamphetamine exposure, polydrug exposure, and poverty on intrauterine growth.

OBJECTIVE: Methamphetamine use among pregnant women is an increasing problem in the United States. Effects of methamphetamine use during pregnancy on fetal growth have not been reported in large, prospective studies. We examined the neonatal growth effects of prenatal methamphetamine exposure in the multicenter, longitudinal Infant Development, Environment and Lifestyle study. DESIGN/METHOD: The Infant Development, Environment and Lifestyle study screened 13808 subjects at 4 clinical centers: 1618 were eligible and consented, among which 84 were methamphetamine exposed, and 1534 were unexposed. Those who were methamphetamine exposed were identified by self-report and/or gas chromatography-mass spectrometry confirmation of amphetamine and metabolites in infant meconium. Those who were unexposed denied amphetamine use and had a negative meconium screen. Both groups included prenatal alcohol, tobacco, or marijuana use, but excluded use of opiates, LSD, PCP or cocaine only. Neonatal parameters included birth weight and gestational age in weeks. One-way analysis of variance and linear-regression analyses were conducted on birth weight by exposure. The relationship of methamphetamine exposure and the incidence of small for gestational age was analyzed using multivariate logistic-regression analyses. RESULTS: The methamphetamine exposed group was 3.5 times more likely to be small for gestational age than the unexposed group. Mothers who used tobacco during pregnancy were nearly 2 times more likely to have small-for-gestational-age infants. In addition, less maternal weight gain during pregnancy was more likely to result in a small-for-gestational-age infant. Birthweight in the methamphetamine exposed group was lower than the unexposed group. CONCLUSIONS: These findings suggest that prenatal methamphetamine use is associated with fetal growth restriction after adjusting for covariates. Continued follow-up will determine if these infants are at increased risk for growth abnormalities in the future.

Adult↗

PubMed2006

Oral health of the methamphetamine abuser.

PURPOSE: The pharmacology of methamphetamine is reviewed, and the effects of methamphetamine use on oral health are described. SUMMARY: Methamphetamine is a highly addictive amphetamine analogue, initially synthesized in 1919. Illicit methamphetamine use leads to devastating effects on health, particularly the dentition. Illegal production of methamphetamine has skyrocketed in recent years, as have the number of users. The chief complaint of methamphetamine users is xerostomia. Without the protective effects of saliva, caries development in these patients is rampant. The typical pattern of decay involves the facial and cervical areas of both the maxillary and mandibular teeth, with eventual progression to frank coronal involvement. The acidic substances used to manufacture this drug have also been implicated as a cause of tooth decay and wear in users, as has bruxism as a result of drug-induced hyperactivity. When possible, these patients should be referred to a dentist to improve their oral health status and minimize the potential for adverse cardiovascular sequelae. Other preventive measures for methamphetamine users include stimulating saliva flow and increasing fluoride supplementation. Pharmacists should also counsel users to avoid carbohydrate-rich soft drinks in favor of water. Oral moisturizers may also be effective. CONCLUSION: Methamphetamine use causes xerostomia secondary to sympathetic central nervous system activation, rampant caries caused by high-sugar intake in the absence of protective saliva, and bruxism as a result of hyperactivity. Practitioners should know how to recognize the signs of and manage the oral health of patients with a history of methamphetamine use.

Humans↗

PubMed2000

Methamphetamine use: hazards and social influences.

Use of methamphetamine, a potent central nervous system stimulant, increased in the early- to mid-1990s in the United States, concentrated in the west, midwest, and south. The use and trade of methamphetamine was facilitated by a fairly simple production process and the involvement of numerous small entrepreneurs as well as drug-trafficking syndicates. National data from the 1994 Drug Abuse Warning network revealed that for the period from 1991 to 1994 methamphetamine use among short-stay hospital patients more than tripled, and methamphetamine-related deaths reported by medical examiner offices nearly tripled. In addition, the Treatment Episode Data Set revealed a 43 percent increase in treatment-program admissions in which clients identified methamphetamine as the primary drug of abuse. Nonetheless, methamphetamine use did not become widespread in the U.S. population. Low-income and unemployed young white men continue to be the group most likely to use methamphetamine, but by the mid-1990s the drug had increased in popularity in more diverse populations and regions. Economic and social pressures experienced by a broad array of Americans may partially explain expanded methamphetamine use; for example, depressed economic conditions in rural and semi-rural areas have contributed to methamphetamine's appeal as a source of income. A "war against drugs" approach has characterized the policy response, with increased criminal justice penalties. A public health approach is recommended, including prevention campaigns, harm-reduction outreach and treatment approaches, and pharmacologic and abstinence-based drug treatment approaches.

Adolescent↗

PubMed1999

Genetic differences in spatial learning between Dark Agouti and Sprague-Dawley strains: possible correlation with the CYP2D2 polymorphism in rats treated neonatally with methamphetamine.

Following neonatal exposure to d-methamphetamine, adult rats have previously been shown to exhibit augmented acoustic startle and spatial learning deficits. d-Methamphetamine is structurally similar to several phenylethylamines that are metabolized by CYP2D6. In humans, allelic differences in the CYP2D6 confer the extensive or poor metabolizer phenotype for the more than three dozen drugs that are members of the CYP2D6-mediated 'debrisoquine/sparteine panel.' An analogous genotype exists with the CYP2D2 gene in rats. Female Dark Agouti rats show the poor metabolizer phenotype, whereas Sprague-Dawley rats show the extensive metabolizer phenotype; male Dark Agouti rats are intermediate. We sought to test the possibility that these strains might exhibit altered d-methamphetamine-induced developmental neurotoxicity. Dark Agouti and Sprague-Dawley litters (11-20 days of age) were given d-methamphetamine or vehicle alone subcutaneously twice daily (15 mg/kg). Offspring were assessed as adults (beginning at 50 days of age) on acoustic startle, straight-channel swimming, and spatial learning and memory in a Morris hidden platform maze. Increases in d-methamphetamine-induced acoustic startle were found in both male and female Dark Agouti rats, but not Sprague-Dawley rats. In the Morris maze, d-methamphetamine-induced spatial navigation deficits were found in both strains among males, suggesting some mechanism other than the CYP2D2 polymorphism. In contrast, among females only the d-methamphetamine-treated Dark Agouti rats showed deficits in spatial navigation. The maze deficits in Dark Agouti females, and enhanced acoustic startle in Dark Agouti females and males, support the hypothesis that the CYP2D2 poor metabolizer phenotype confers increased vulnerability to d-methamphetamine-induced developmental neurotoxicity, indicating that the parent drug rather than a CYP2D2-mediated metabolite is responsible for this behavioural defect--which occurs in adults who had been exposed to d-methamphetamine during the neonatal period.

Animals↗

PubMed1989

Cocaine- and methamphetamine-related deaths in San Diego County (1987): homicides and accidental overdoses.

Cocaine- and methamphetamine-related homicides and fatal accidental overdoses in San Diego County were studied retrospectively for the 1987 calendar year. Cocaine was involved in 66 cases (39 homicides, 27 accidental overdoses), methamphetamine in 32 cases (23 homicides, 9 accidental overdoses), and a combination of cocaine and methamphetamine in 10 cases (4 homicides, 6 accidental overdoses). The composite for cocaine-related deaths was a 30-year-old black man in whom was also found at least 1 other drug, usually ethanol or morphine. The composite for methamphetamine-related deaths was a 32-year-old Caucasian man who used methamphetamine with at least 1 other drug (usually ethanol). For cases involving both cocaine and methamphetamine, the composite was a 36-year-old Caucasian man in whom was also found at least 1 other drug, usually ethanol, codeine, or morphine. Mean tissue concentrations of cocaine and benzoylecgonine were significantly higher in accidental overdoses than in homicides except for cocaine concentrations in liver, which did not differ significantly between the two groups. For methamphetamine-related deaths there was no significant difference between mean tissue concentrations in accidental overdoses and in homicides. Cocaine or methamphetamine or both were involved in approximately one third of homicides in San Diego County in 1987, and when fatal accidental overdoses were included, cocaine was involved in twice as many cases as methamphetamine.

Accidents↗

PubMed1989

[Immunohistochemical study on the mechanism of excretion of methamphetamine].

Many methods of analysis are available to the forensic toxicologist for determining the amount of methamphetamine within human tissues, but few have the potential of histochemistry for enabling the precise site of excretion of methamphetamine to be defined. We have established a method for the demonstration of methamphetamine by immunohistochemistry, and applied this method for showing morphologically the disposition of methamphetamine. The following cells in the tissues of methamphetamine-intoxicated mice gave a strong positive reaction of the localization, which was thought to be the histological evidence of excretion of this drug: epithelial cells of the distal part of the renal tubule and of the collecting tubule, transitional epithelial cells of the bladder, liver parenchymal cells, epithelial cells of the striated duct of the salivary gland, parietal cells of the gastric gland, part of epithelial cells of the distal portion of the large intestine, secretory cells and part of epithelial cells of the ductal portion of the sweat gland, alveolar cells of the mammary gland, secretory cells of the sebaceous gland and hair medulla and cortex. These results indicated passive diffusion of methamphetamine across membranes of the cells of the distal tubule and collecting tubule of the kidney, of the bladder and of the striated duct of the salivary gland. In the parietal cells of the gastric gland, part of epithelial cells of the distal portion of the large intestine and secretory cells of the sweat gland, methamphetamine was thought to be stored and subsequently released. In the mammary gland, methamphetamine was found to be combined with casein and excreted by exocytosis. Accumulation of methamphetamine in the hair was supposed to be chiefly due to the penetration of this drug derived from tissue fluid and sebum.

Animals↗