EXPERIMENTAL STUDY ON PATHOGESIS OF ACUTE MYOCARDIAL INFARCTION-ROLE OF LOCAL AND NEUROHUMORAL FACTORS-

冠状动脉造影不能充分预测急性心肌梗死（AMI）后血栓闭塞的部位。此外，突发性冠状动脉闭塞的机制仍然是完全未知的。本研究的目的是通过提高不同类型动脉硬化兔的血液凝固性来诱导急性心肌梗死。本研究选用平均年龄为18月龄的WATANABE遗传性高脂血症兔39只。77只家兔间歇或连续饲喂胆固醇8-12个月，正常家兔9只。为了提高血液凝固性，将罗素毒蛇毒液（RVV: 150马克杯/公斤）腹腔注射，同时静脉注射血清素（100马克杯/公斤）或血管紧张素II （Ang: 20-40马克杯/公斤），持续2天。9只正常兔中有2只，29只WHHL兔中有7只，67只喂胆固醇的兔中没有发现典型的AMI病变（小于48小时），这些兔子都接受了血清素或血管紧张素的RVV。29只WHHL兔中有5只发现闭塞性冠状动脉血栓形成，而胆固醇喂养兔中没有发现血栓形成。5例冠状动脉血栓中仅有2例与冠状动脉粥样硬化相关，但在血栓形成部位未发现斑块破裂或富含巨噬细胞的斑块。与注射RVV和5 -羟色胺的WHHL兔相比，30mg /kg可促进WHHL兔主动脉血栓形成，并伴有节段性内侧坏死和斑块边缘增厚内膜破裂（p<0.01）。巨噬细胞斑块与主动脉血栓形成无密切关系。因此，我们得出结论，AMI病变很少由高凝性聚集血栓的血栓栓塞引起，但与冠状动脉粥样硬化斑块破裂无关，而血管紧张素II引起的血压升高促进主动脉血栓形成，与WHHL兔的中间坏死和增厚内膜破裂有关。少

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 … More 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