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急性缺血心肌的保护:冠状动脉再灌注的利弊

The protection of the acute ischemic myocardium: merits and demerits of the coronary reperfusion.

作者信息

Miura M, Matsu-Oka H, Kanazawa T

机构信息

Second Department of Internal Medicine, Akita University School of Medicine, Japan.

出版信息

Jpn Circ J. 1989 Sep;53(9):1084-91. doi: 10.1253/jcj.53.1084.

Abstract

At first, in order to know the causes of reperfusion injury, we studied myocardial injury by reperfusion in comparison with by Ca overloading, and the salvage of the myocardium from reperfusion and from Ca overloading by Ca antagonist, diltiazem (DIL), in 52 anesthetized open-chest dogs. In myocardial mitochondria (Mit), Ca content was increased and Mg content and oxidative phosphorylation (State III) were decreased both by 120 min reperfusion after 60 min occlusion and by Ca overloading. Ca and Mg contents and oxidative phosphorylation of Mit were similarly changed by reperfusion as by Ca overloading. Electron-microscopically, myocardial injury by Ca overloading resembled reperfusion injury. Therefore, Ca inflow to myocardial cells may be one of the determinant factors which induce reperfusion injury. Although myofibrils were disorganized and contraction band necrosis appeared in these two types of myocardial injury, amorphous densities and glanular densities which indicated the irreversible injury of Mit appeared only in reperfusion injury. Then, the myocardial injury by Ca overloading is suspected of being mainly composed of the injury of myofibrils. The myocardial injury by reperfusion and by Ca overloading was prevented by DIL. These facts suggest that DIL may suppress Ca inflow and Mg outflow to myocardial cells. Second, to know the effect of positive inotropic agents on pump failure in acute myocardial infarction, we studied the effect of dobutamine (DOB) on the ischemic myocardium and the salvage of the ischemic myocardium from DOB-induced injury by DIL in 39 anesthetized open-chest dogs. After occlusion, the regional mechanical function of the acute ischemic myocardium was rapidly lost and % systolic shortening was negative level. In this situation, myocardial Pco2 quickly increased and myocardial pH rapidly decreased. These parameters reached peak level after 20 min occlusion. Then, paradoxical improvement phenomenon appeared so that Pco2 decreased and pH increased after that. Myocardial blood flow measured by thermocouples was stable at almost 10% of the preoccluded level for a 90 min occlusion. These data suggest that anaerobic metabolism and residual aerobic metabolism can not supply the ischemic myocardium with enough energy and that irreversible injury may appear in the ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

首先,为了了解再灌注损伤的原因,我们在52只麻醉开胸犬中,研究了再灌注所致心肌损伤与钙超载所致心肌损伤的情况,以及钙拮抗剂地尔硫䓬(DIL)对再灌注及钙超载所致心肌损伤的挽救作用。在心肌线粒体(Mit)中,60分钟闭塞后120分钟再灌注以及钙超载均使钙含量增加,镁含量及氧化磷酸化(状态III)降低。Mit的钙、镁含量及氧化磷酸化在再灌注时的变化与钙超载时相似。电镜下,钙超载所致心肌损伤类似于再灌注损伤。因此,钙流入心肌细胞可能是诱导再灌注损伤的决定性因素之一。虽然在这两种心肌损伤中肌原纤维均紊乱且出现收缩带坏死,但仅在再灌注损伤中出现了表明Mit不可逆损伤的无定形致密物和颗粒状致密物。那么,怀疑钙超载所致心肌损伤主要由肌原纤维损伤构成。DIL可预防再灌注及钙超载所致心肌损伤。这些事实提示,DIL可能抑制钙流入及镁流出心肌细胞。其次,为了解正性肌力药物对急性心肌梗死泵衰竭的影响,我们在39只麻醉开胸犬中研究了多巴酚丁胺(DOB)对缺血心肌的作用以及DIL对DOB所致缺血心肌损伤的挽救作用。闭塞后,急性缺血心肌的局部机械功能迅速丧失,收缩期缩短百分比呈负值。在此情况下,心肌Pco2迅速升高,心肌pH迅速降低。这些参数在闭塞20分钟后达到峰值水平。然后,出现矛盾性改善现象,此后Pco2降低,pH升高。用热电偶测量的心肌血流量在90分钟闭塞期间稳定在闭塞前水平的近10%。这些数据提示,无氧代谢和残余有氧代谢不能为缺血心肌提供足够能量,且缺血心肌可能出现不可逆损伤。(摘要截选至250词)

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