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

目的探讨急性心肌梗死合并严重泵衰竭的机制。我们注意到非梗死心肌代谢的改变。（方法）结扎犬左回旋支（LCX）造成急性缺血心肌，测定血流动力学、心肌血流量（MBF）和心输出量（CO）。将犬分为左回旋支结扎后60 min升主室收缩压（LVSP）下降<70%（泵衰竭组）和LVSP保持在70%以上（非抑郁组）两组，观察了儿茶酚胺（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害的影响。D组部分动物于LCX结扎后90 min开始静脉滴注DOA、DOB和AMN，持续30 min。用离心法从非梗塞心肌（NIZ）和梗塞心肌（IZ）中提取肌浆网（SR）和线粒体（Mt）， ...更多信息 两组均于LCX结扎后120 min处死。电镜观察各组心肌细胞形态。（结果）D组大鼠NIZ的CO和MBF明显降低;与ND组相比，D组NIZ SR中Ca-ATPase活性明显降低，而SR蛋白质和呼吸活性无明显变化，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。呼吸活动和电子传递酶的活性恢复，以及血流动力学、CO和MBF的改善。另一方面，在AMN给药时，线粒体功能恢复，而血流动力学和MBF没有改善。形态学分析D组NIZ的Mt轻度肿胀融合，DOA组Mt轻度肿胀融合。DOB组和AMN组。（结论）急性心肌梗死时发生严重泵衰竭与梗死面积有关，严重泵衰竭时心肌血流量减少，心肌SR和Mt代谢受损，导致心源性休克心脏恶性循环。DOA和DOB可能通过改善冠脉血流而打破恶性循环，AMN可能直接作用于心肌。少

(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