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心肌缺血再灌注后的血清肌酸磷酸激酶(CPK)酶。

Serum CPK enzymes in myocardial ischemia followed by reperfusion.

作者信息

Sharma G P, Hornady G

出版信息

Adv Myocardiol. 1980;2:383-96.

PMID:7423052
Abstract

Results from 30 experiments designed to correlate changes in serum creatine phosphokinase (CPK) enzyme concentration, myocardial tissue CPK enzyme content, and myocardial ultrastructure following myocardial ischemia and subsequent reperfusion are presented. The highest and most remarkable change is seen in 1 hr of ischemia followed by 24 hr of reperfusion. In this group, myocardial tissue CPK content is maintained during ischemia as well as reperfusion, indicating adequate enzyme synthesis to offset the enzyme leaking into blood serum simultaneously. The myocardial cells also show recovery in ultrastructure after reperfusion. The finding indicates that short periods of myocardial ischemia, such as this, are compatible with cell survival if adequate perfusion is restored early. Change in serum CPK enzymes, in this case, may indicate successful revascularization rather than development of an infarct.

摘要

本文展示了30项实验的结果,这些实验旨在关联心肌缺血及随后再灌注后血清肌酸磷酸激酶(CPK)酶浓度、心肌组织CPK酶含量和心肌超微结构的变化。在缺血1小时后再灌注24小时时,出现了最高且最显著的变化。在该组中,心肌组织CPK含量在缺血和再灌注期间均得以维持,这表明有足够的酶合成以抵消同时泄漏到血清中的酶。再灌注后心肌细胞的超微结构也显示出恢复。这一发现表明,像这样短时间的心肌缺血,如果早期恢复足够的灌注,与细胞存活是相容的。在这种情况下,血清CPK酶的变化可能表明血管再通成功而非梗死形成。

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Adv Myocardiol. 1980;2:383-96.
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