| Project/Area Number |
61570290
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Legal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
MATOBA Ryoji (Associate Professor) Osaka University Medical School, 医学部, 助教授 (20107056)
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| Co-Investigator(Kenkyū-buntansha) |
FUJITANI Noboru (Assistant) Osaka University Medical School, 医学部, 助手 (10156888)
SHIKATA Ichiro (Professor) Osaka University Medical School, 医学部, 教授 (10035371)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1987: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1986: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | methamphetamine / cardiac injury / catecholamine / B-blocker / Ca-antagonist / Ca-antagonisr / 心筋症 |
|---|
| Research Abstract |
To investigate the effects of long-term mechamphetaminc(MA) administration in animals. MA 5. 10. 20 mg/kg b.w. was injected to ddy male mice 6 times per week for 2 or 4 weeks. In microscopic observations there were the findings: hypertrophy. atrophy. eosinophilic changes, vacuolation contraction band nccrosis and disarray of myofibers. minimum patchy fibrosis. interstitial edema and infiltrations of small round cells. These lesions were mainly seen at the left ventricle and the septum except disarray of myotibers which was prominent at the triangle region. Electorn microscopy revealed further appearance of irregularity of sarcolomma, hypercontraction of sarcomere, thickning of % band. increase in myofibrillar elements and mitochondria and dilatation of the sarcomplasmic reticuliums. Dissapearance of myofibrils. degenerations of mitochondia and myofibrillar disarray were sometimes seen. Furthermore. many single membrane vesicles were sometimes observed bancath the sarcolemma. Thesed sur
… More
face vesiclees were similar to dilated sarcoplasmic reticulums in size, sometimes fused with sarcolomma and seen in the basement membrane. inthe cndothelial cells and in the capillary lumen. In general, the severity of these cardiac lesions were in proportion to both the doso and the duration of MA administrated. but disarray of myofibers were rather found frequently in the group administered smaller dose of MA. We then compared the lesions by MA with those after administration of catecholamine. and also examined the effect of -blocker and Ca-antagonist. The cardiac lesions after norepincphrine administration were similar to those after MA administration but to a limited extent. On the contrally. premedication of propranolol and verapamil prevented the appcarance of the cardiac lesion. isolorm pattern of cardiac myosin of the mice administered MA as by pyrophosphate gei cicotrophoresis showed to so remarkable difference from that of controll mice. Thus. various cardiac lesions found in MA abusers seemed to be explained by the cardiac toxicity of MA by itself. Furtheermore. our result suggests that. MA induces cardiac injury through catecholamine released from nerve endings. and possibly caleium everioad may be also involved. Less
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