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结扎21条犬冠状动脉左前降支后18～24小时,于左室前壁缺血或梗塞处取材行组织化学和电镜观察,结果表明心肌内塘原减少或消失,碱性磷酸酶和三磷酸腺苷酶反应阳性的毛细血管数量减步或分布不均,后者显示心肌内微循环障碍。同时表明心肌内琥珀酸脱氢酶的反应颗粒明显减少或消失,是心肌缺血较敏感而可靠的指标。梗塞灶周围心肌出现脂肪变性。电镜观察显示心肌线粒体内出现无定形致密颗粒和心肌内形成断裂凝聚带为心肌早期坏死的主要形态依据。心肌内毛细血管内皮细胞严重受损和微循环障碍既为心肌缺血的后果,又可加重心肌的缺血性损害。
Ligation of 21 canine coronary anterior descending branch after 18 to 24 hours in the anterior ischemic or infarcted left anterior wall of the material taken line histochemistry and electron microscopy results showed that the reduction of myocardial Tong Tong Yuan or disappeared, alkaline phosphatase and adenosine triphosphate The number of reactive-positive capillaries diminished or unevenly distributed, the latter showing intramyocardial microcirculation. At the same time, it indicates that the intramyocardial succinate dehydrogenase reaction particles significantly reduce or disappear, which is a sensitive and reliable indicator of myocardial ischemia. Myocardial infarction around the fatty degeneration. Electron microscopy showed myocardial mitochondria in the presence of amorphous dense particles and the formation of myocardial infarction in the coagulation zone as the main form of myocardial necrosis. Myocardial capillary endothelial cell damage and microcirculation are both the consequences of myocardial ischemia, but also aggravate myocardial ischemic damage.