1994 Fiscal Year Final Research Report Summary
EXPERIMENTAL STUDY ON PATHOGESIS OF ACUTE MYOCARDIAL INFARCTION-ROLE OF LOCAL AND NEUROHUMORAL FACTORS-
| Project/Area Number |
04454273
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | NAKAMURA-GAKUEN COLLEGE |
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Principal Investigator |
NAKAMURA Motoomi THE GRADUATE SCHOOL OF HEALTH AND NUTRITION SCIENCES,NAKAMURA-GAKUEN COLLEGE,PROFESSOR, 大学院・栄養科学研究所, 教授 (60037322)
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| Co-Investigator(Kenkyū-buntansha) |
ABE Shimako DEPARTMENT OF FOOD AND NUTRITION,NAKAMURA-GAKUEN COLLEGE,ASSOCIATE, 家政学部, 助手 (60192994)
HARA Takayuki DEPARTMENT OF FOOD AND NUTRITION,NAKAMURA-GAKUEN COLLEGE,ASSISTANT PROFESSOR, 家政学部, 助教授 (10164998)
AOMINE Masahiro DEPARTMENT OF FOOD AND NUTRITION,NAKAMURA-GAKUEN COLLEGE,PROFESSOR, 家政学部, 教授 (60091261)
TANIGUCHI Misako DEPARTMENT OF FOOD AND NUTRITION,NAKAMURA-GAKUEN COLLEGE,PROFESSOR, 家政学部, 教授 (70069764)
FUJITA Mamoru DEPARTMENT OF FOOD AND NUTRITION,NAKAMURA-GAKUEN COLLEGE,PROFESSOR, 家政学部, 教授 (60037471)
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| Project Period (FY) |
1992 – 1994
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| Keywords | Medial necrosis / Aortic thrombosis / WHHL / Hyperlipidemia / Acute myocardial infarction / Disruption of thickened intima / Russel's viper venom / Angiotensin II |
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| Research Abstract |
Coronary angiography cannot adequately predict the site of a subsequent thrombotic occlusion following an acute myocardial infarction (AMI). In addition, the mechanisms of sudden coronary occlusion still remain completely unknown. The aim of the present study is to induce AMI experimentally by increasing blood coagulability in various types of arteriosclerotic rabbits.
Thirty-nine WATANABE heritable hyperlipidemic rabbits (WHHL) with an average age of 18 months, were used in this study. Seventy-seven rabbits were fed cholesterol either intermittently or continuously for 8-12 months and 9 normal rabbits were used. To increase blood coagulability, Russel's viper venom (RVV : 150mug/kg) was administered intraperitoneally with an intravenous injection of either serotonin (100mug/kg) or angiotensin II (Ang : 20-40mug/kg) for 2 days. A typical AMI lesion (less than 48 hours old) was found in 2 out of the 9 normal rabbits, seven of 29 WHHL rabbits and none of 67 cholesterol-fed rabbits who all
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received RVV with serotonin or angiotensin. Occlusive coronary thrombosis was found in 5 of the 29 WHHL rabbits but in none of the cholesterol-fed rabbits. Only 2 of the 5 coronary thrombi were associated with coronary atherosclerosis, but neither any plaque-ruptures nor macrophage rich plaque was found at the thrombotic site. Ang (30mug/kg) promoted aortic thrombosis associated with segmental medial necrosis and a disruption of the thickened intima at the edge of the plaque in the WHHL rabbits, when compared with that of the WHHL rabbits which received RVV and serotonin (p<0.01). No close correlation between the macrophage rich plaque and aortic thrombosis was confirmed.
We thus conclude that AMI lesions were rarely produced by a thrombo-embolism of the aggregated thrombi due to hypercoagulability, but not associated with plaque-rupture of the coronary atherosclerosis, while the elevation of blood pressure by angiotensin II promoted aortic thrombosis in association with medial necrosis and an intimal disruption of the thickened intima in the WHHL rabbits concerned. Less
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