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犬冠状动脉血栓形成致急性心肌梗塞实验模型的研究

Experimental Model of Acute Myocardial Infarction Induced by Coronary Arterial Thrombosis in Dogs

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【作者】 傅良武赵华月郭志凌熊一力

【Author】 Fu Liangwu; Zhao Huayue; Guo Zhiling et al (Department of Internal Medicine, Tongji Hospital, Tongji Medical University, Wuhan 430030)

【机构】 武汉同济医科大学附属同济医院内科

【摘要】 采用冠状动脉(简称冠脉)内膜微电流刺激法进行犬冠脉血栓形成(CAT)致急性心肌梗塞(AMI)模型的实验研究。以冠脉血流量、血栓湿重和形态证实了CAT形成,病理切片显示血栓构成与人类动脉血栓相似。心外膜心电图、血清肌酸激酶(CPK)及心肌病检结果表明有心肌缺血和梗塞病灶产生,TXB和TXB/6-酮-PGF1α比值增高可能促发CAT,cAMP增高诱发心律失常。AMI首先损害心脏舒张性能,继而损害收缩性能,导致心脏泵功能下降。

【Abstract】 An experimental animal model for coronary arterial thrombosis(CAT) inducing acute myocardial infarction(AMI) was established by delivery of low amperage electric current to the intimal. surface of artery in dogs. The results showed that the coronary blood flow(CBF)was decreased to zero, the plasma TXB2 concentration and ratio of TXB2 over 6keto-PGFwere increased, the plasma cAMP and CPK level were increased. In epicardialECG, the ST segment was elevated in association with appearance of Q wave. The thrombus was rich in platelet, with wet weight being 31.4±9.5g. It occupied the lumina of left circumflex coronary artery(LCX) and resulted in the formation of ischemic and infarct focus of heart. The myocardial ischemic size and infarct size amounted to 35.0±8.1%and 20.0±7.4%of left ventricular(LV)mass respectively. AMI and the elevation of plasma cAMP level might provoke ventricular fibrillation. After AMI, the LV dastolie function decreased first, followed by deterioration of the LV systolic function leading to failure of ventricular pumping function.

【基金】 湖北省自然科学基金
  • 【文献出处】 同济医科大学学报 ,ACTAUNIVERSITATIS MEDICTNAE TANGJI , 编辑部邮箱 ,1995年01期
  • 【分类号】R543.31
  • 【被引频次】11
  • 【下载频次】110
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