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心肌梗死中交感神经活动的病理生理意义研究。

Studies on pathophysiological significance of sympathetic activity in myocardial infarction.

作者信息

Yao T

出版信息

Jpn Circ J. 1975 Dec;39(12):1293-303. doi: 10.1253/jcj.39.1293.

Abstract

In an attempt to elucidate the pathophysiological significance of the sympathetic hyperactivity in the acute stage of myocardial infarction, the author observed changes in the urinary excretion of CA, the CA content in the myocardium and the hemodynamics in both clinical and experimental myocardial infarction, and the following were found: 1) In clinical myocardial infarction, the urinary excretion of CA was markedly increased immediately after an attack, and the assay of myocardial specimens form the autopsied patients of acute myocardial infarction revealed that the CA content in the non-infarcted area was lower than that in the infarcted area. 2) In the experiments on rabbits with ligated coronary artery, the increase in cardiac contractility and rise in blood pressure in response to CA was supressed after the ligation of coronary artery. In the early stage of experimental myocardial infarction, the decrease of myocardial CA content in the non-infarcted area was, as in autopsied patients, predominant over the decrease of that in the infarcted area. In the chronic stage (more than one week after the coronary ligation), the CA content in the infarcted area showed further decrease, but in the non-infarcted area it was recovered to the level in the control animals. The uptake of exogenous NA into the non-infarcted area decreased in the acute stage, and in the infarcted area it showed marked decreased in the chronic stage. The urinary excretion of CA was increased in the acute stage of myocardial infarction. 3) The administration of betamethasone suppressed the decrease in the CA content in the myocardium following the ligation of coronary artery. Based on these findings, the author came to a postulation that the sympathetic hyperactivity which is suggested by increased urinary excretion of CA and decreased CA content in the myocardium results from the reasonable biophylactic reaction so as to supplement the cardiac hypofunction derived from myocardial infarction.

摘要

为阐明心肌梗死急性期交感神经过度活跃的病理生理意义,作者观察了临床和实验性心肌梗死患者尿儿茶酚胺(CA)排泄量、心肌CA含量及血流动力学的变化,结果如下:1)临床心肌梗死患者发作后尿CA排泄量立即显著增加,对急性心肌梗死尸检患者心肌标本的检测显示,非梗死区CA含量低于梗死区。2)在结扎冠状动脉的兔实验中,冠状动脉结扎后,CA引起的心脏收缩力增强和血压升高受到抑制。在实验性心肌梗死早期,非梗死区心肌CA含量的降低如尸检患者一样,比梗死区更为明显。在慢性期(冠状动脉结扎后一周以上),梗死区CA含量进一步降低,但非梗死区恢复到对照动物的水平。急性期非梗死区对外源性去甲肾上腺素(NA)的摄取减少,慢性期梗死区摄取显著减少。心肌梗死急性期尿CA排泄量增加。3)给予倍他米松可抑制冠状动脉结扎后心肌CA含量的降低。基于这些发现,作者提出一种假设,即尿CA排泄量增加和心肌CA含量降低所提示的交感神经过度活跃是一种合理的生物防御反应,以补充心肌梗死导致的心脏功能减退。

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