Methamphetamine Induced Toxicities in Rats and Human

• Main Authors: Pu, Chang-En, 蒲長恩
• Other Authors: Shaw, Kai-Ping
• Format: Others
• Language: zh-TW
• Published: 1994
• Online Access: http://ndltd.ncl.edu.tw/handle/66700949597882443626

碩士 === 國防醫學院 === 解剖學研究所 === 82 === Methamphetamine(MAP) is currently the major illicit drug in Taiwan. The fatal victims due to MAP abuse are increasing. The purposes of this study are to establish a database of these fatalities for epidemiology study and to establish animal models of self-administration (ingestion) of MAP that mimic the behaviors of human and to compare the MAP-induced toxicities in rats to that of human. 50 MAP- related fatalities from 1990 to 1992 were collected from Forensic Medicine Center. The definite lesions are hemorrhagic pulmonary edema (72%, n=36). 36 out 50 autopsy cases of The MAP concentration distribution from 0.36 to 80.70 μg/ml (mean 13.21 ±17.67 μ g/ml) in blood and 0.52 to 107.00 μ g/ml (mean 25.89 ±31.46 μ g/ml) in urine, the ratio is 1:2. Rats were fed with MAP (0.005-0.2 mg/ml) for a period of time. MAP concentration of ingestion, inhalation, urine excretion and blood level were monitored by Gas Chromatography / Mass Spectrophtometer method. The quantity of daily intake (ingestion) and output (urine) of MAP of self- administration rats fed with MAP 0.05, 0.1, 0.2 mg/ml were correlated. Chronic MAP ingestion with the concentration above 0.05 mg/ml induced intoxication. MAP concentration of blood and urine of rats after self-administration at 30 days are 4.68± 3.03 and 37.79±4.21 μ g/ml, the ratio is 1: 8. Chronic self-administrated and MAP rats showed delayed response to MAP induced hyperthermia and vasomotor effects. Spinal rats(T1) showed no significant reduce of hyperthermia induced by MAP, with low motality rate and mild hemorrahage pulmonary edema. These data shows that fatalities, hyperthermia and neurogenic pulmonary edema induced by MAP are correlated. These data are eligible for us to evaluate the progress of MAP-related fatalities and to explain the pathogenesis of MAP-induced toxicities.