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[心脏缺血性挛缩的动力学与发病机制]

[Dynamics and pathogenesis of ischemic contracture of the heart].

作者信息

Otverchenko V N, Bulgakov V G, Volkova I A, Bilenko M V

出版信息

Kardiologiia. 1984 Aug;24(8):100-4.

PMID:6492572
Abstract

In experiments on 34 dogs, the authors studied myocardial rigidity, ATP levels and Ca2+-accumulating function of the membranes of the sarcoplasmic reticulum (SR) in the external (subepicardial) and internal (subendocardial) layers of the myocardium at 1 and 2 h of total ischemia at 37 degrees C and also 30 min after cardiac reperfusion by heterotopic transplantation. It was revealed that contracture changes in ischemia first affect the internal and then the external layer of the myocardium which corresponds to the initial and completed phases of ischemic contracture (IC) of the heart, correspondingly. IC of the heart is irreversible and in cases of total contracture of all layers of the myocardium (the completed phase) the heart loses contractile function. Changes in the contractility in the external and internal layers of the myocardium show a stronger inverse correlation with the capacity of SR membranes to absorb Ca2+ rather than with ATP levels in the tissues which indicates an essential role of the Ca2+ accumulating function of SR in the pathogenesis of IC.

摘要

在对34只狗进行的实验中,作者研究了在37℃完全缺血1小时和2小时以及通过异位移植心脏再灌注30分钟后,心肌外层(心外膜下)和内层(心内膜下)的心肌僵硬度、三磷酸腺苷(ATP)水平以及肌浆网(SR)膜的钙离子蓄积功能。结果显示,缺血时的挛缩变化首先影响心肌内层,然后是外层,这分别对应于心脏缺血性挛缩(IC)的初始阶段和完成阶段。心脏的IC是不可逆的,在心肌所有层完全挛缩(完成阶段)的情况下,心脏会失去收缩功能。心肌外层和内层收缩性的变化与SR膜吸收钙离子的能力呈现更强的负相关,而非与组织中的ATP水平相关,这表明SR的钙离子蓄积功能在IC发病机制中起着重要作用。

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