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Mechanisms of Severe Pump Failure in Acute Myocardial Infarction and Alteration of Cardiac Metabolisms.

急性心肌梗塞严重泵衰竭的机制和心脏代谢的改变。

基本信息

批准号：
01570503
负责人：
KATAGIRI Takashi
金额：
$ 1.28万
依托单位：
Showa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

项目摘要

(Objects) We studied the mechanism of severe pump failure associated with acute myocardial infarction. We gave attention to the alteration of metabolism in non-infarcted myocardium. (Methods) Acute ischemic myocardium was produced by ligation of LCX in canine heart, and hemodynamics, myocardial blooD flow (MBF) and cardiac output (CO) were measured. Dogs were divided into two groups of which lift ventricular systolic pressure (LVSP) decreased less than 70% to prior value at 60 min after LCX ligation (pump failure : D group), and LVSP was kept higher than 70% as non-depressive group (ND group).And the effects of catecholamine (dobutamine : DOA and DOB) and phosphodiesterase inhibitor (AMN) on metabolic impairment in non-infarcted myocardium. DOA, DOB and AMN were dripped intravenously in some of D group for 30 min from 90 min after LCX ligation. Sarcolasmic reticulum (SR) and mitochondria (Mt) were extracted by centrifuge method from non-infarcted (NIZ) and infarcted heart muscle (IZ) a … More t 120 min after LCX ligation in both groups. Each myocardial cells were observed with electron microscopy. (Results) CO and MBF of NIZ were decreased significantly in D group. Ca-ATPase activity in SR from NIZ in D group was markedly reduced without degradation of SR protein and respiratory activity, activities of electron transport enzymes in Mt from NIZ were decreased too, compared with those of NIZ in ND group. For the purpose of improve the disturbed hemodynamics, DOA and DOB were administerd in some of D group. Recovery in respiratory activity and electron transport enzymes activities were found in Mt from NIZ, together with the improvement of hemodynamics, CO and MBF in NIZ. On the other hand in administration of AMN, mitochondrial function was restored without improvement of hemodynamics and MBF. In morphological analysis, Mt from NIZ in D group were slightly swollen and fused, but these changes were mild in DOA. DOB and AMN group. (Conclusion) These results suggest that occurrence of severe pump failure in acute myocardial infarction is due to the size of infarcted area in previous papers, metabolic impairment of SR and Mt in NIZ were demonstrated with reduction in MBF under severe pump failure which leads to malicious cycle in cardiogenic shocked heart. DOA and DOB showed the possibility to break the malicious cycle by improving coronary blood flow and AMN may be work n myocardium directly. Less

（目的）探讨急性心肌梗死并发严重泵功能衰竭的发生机制。我们关注非梗死心肌代谢的改变。（方法）结扎犬心脏LCX形成急性缺血心肌，测定血流动力学、心肌血流量（MBF）、心输出量（CO）。将犬分为两组，左心室收缩压（LVSP）在LCX结扎后60 min较术前下降小于70% （D组），无抑郁组（ND组）LVSP维持在70%以上。儿茶酚胺（多巴酚丁胺：DOA和DOB）和磷酸二酯酶抑制剂（AMN）对非梗死心肌代谢损伤的影响。D组部分患者自LCX结扎后90 min开始静脉滴注DOA、DOB和AMN，滴注时间为30 min。在LCX结扎后1 ~ 120 min，用离心分离法分别从非梗死心肌（NIZ）和梗死心肌（IZ）中提取肌痉挛网（SR）和线粒体（Mt）。电镜观察各组心肌细胞。（结果）D组NIZ的CO和MBF明显降低。与ND组相比，D组NIZ产的SR中ca - atp酶活性显著降低，但SR蛋白和呼吸活性均未发生降解，Mt中电子传递酶活性也明显降低。为改善血流动力学紊乱，D组部分患者给予DOA和DOB。呼吸活性和电子传递酶活性恢复，血流动力学、CO和MBF改善。另一方面，给药AMN后，线粒体功能恢复，但血流动力学和MBF没有改善。形态学分析中，D组NIZ的Mt轻微肿胀和融合，但DOA的这些变化是轻微的。DOB和AMN组。（结论）上述结果提示急性心肌梗死严重泵衰竭的发生与梗死面积大小有关，NIZ的SR和Mt代谢障碍与严重泵衰竭下MBF降低有关，导致心源性休克心脏恶性循环。DOA和DOB显示了通过改善冠状动脉血流打破恶性循环的可能性，AMN可能直接在心肌中起作用。少