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

(目的)探讨急性心肌梗死并发严重泵衰竭的机制。我们注意到非梗死区心肌代谢的改变。(方法)结扎左旋支制作犬急性心肌缺血模型，测定血流动力学、心肌血流量(MBF)和心输出量(CO)。将犬分为两组，结扎左冠状动脉后60min左心室收缩压降至70%以下(泵衰竭组：D组)，非抑郁组(ND组)维持在70%以上，观察儿茶酚胺(多巴酚丁胺、道布)和磷酸二酯酶抑制剂对非梗死区心肌代谢损伤的影响。D组部分结扎后90min开始静脉滴注DOA、道布和氨基精氨酸氨基转移酶30min。用离心法从非梗死区(NIZ)和梗死区(IZ)心肌(…)中提取肌浆网(SR)和线粒体(MT)。两组均在Lcx结扎后120min以上。用电子显微镜观察各心肌细胞的形态。(结果)D组NIZ的CO和MBF显著降低。与ND组比较，D组NIZ组SR的Ca-ATPase活性显著降低，而SR蛋白和呼吸活性无明显变化，线粒体电子传递酶活性也降低。D组部分患者给予多巴酚丁胺和道布治疗，改善血流动力学紊乱。NIZ组呼吸活动和电子传递酶活性恢复，血流动力学、CO和MBF均有改善。给予AMN后，线粒体功能恢复，但血流动力学和MBF未见改善。形态学分析显示，D组NIZ的mt轻度肿胀融合，DOA改变较轻。道布和AMN组。(结论)急性心肌梗死严重泵衰竭的发生与心肌梗死面积的大小有关，在严重泵衰竭的情况下，NIZ的SR和MT代谢受损，MBF下降，从而导致心源性休克心脏的恶性循环。DOA和道布提出了通过改善冠脉血流量来打破这种恶性循环的可能性，AMN可能直接作用于心肌。较少

(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