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缺血再灌注对离体大鼠心脏线粒体接触位点的影响。

The effect of ischemia and reperfusion on mitochondrial contact sites in isolated rat hearts.

作者信息

Bakker A, Goossens F, De Bie M, Bernaert I, Van Belle H, Jacob W

机构信息

Department of Medicine, University of Antwerp, Belgium.

出版信息

Histol Histopathol. 1995 Apr;10(2):405-16.

PMID:7599437
Abstract

Contact sites may be described as energy channels between the mitochondria and the cytosol, created by fusion of the inner and the outer mitochondrial membranes, and their number depends highly on the energy state of the cell. The aim of the present study was to examine the early changes of ischemia and reperfusion on the number of mitochondrial contact sites. Therefore isolated rat hearts were subjected to short periods of ischemia followed by reperfusion. The left ventricular pressure (LVP), the contractility (dP/dtmax) and the heart rate were measured. The number of contact sites was morphometrically evaluated. As the flow was stopped, LVP, dP/dtmax and HR declined rapidly and became undetectable after 2 min of ischemia. The number of contact sites fell to a minimum after 10 min of ischemia after an initial increase (1 min of ischemia). A 15 min ischemic period resulted in a high number of contact sites which decreased again after 20 min of ischemia. Reperfusion after 2 min of ischemia caused an immediate functional recovery and a high presence of contact sites. After 15 min of reperfusion, all values returned to control values. Reperfusion after 10 min of ischemia resulted in a slow recovery of the number of contact sites and after 15 min of ischemia the number of contact sites remained low upon reperfusion. We may conclude that mitochondria lose the ability to form contact sites after more than 15 min of ischemia and this might be a first indication of irreversible injury.

摘要

接触位点可被描述为线粒体与细胞质之间的能量通道,由线粒体内外膜融合形成,其数量在很大程度上取决于细胞的能量状态。本研究的目的是检测缺血和再灌注对线粒体接触位点数量的早期影响。因此,对离体大鼠心脏进行短时间缺血后再灌注处理。测量左心室压力(LVP)、收缩性(dP/dtmax)和心率。通过形态计量学评估接触位点的数量。随着血流停止,LVP、dP/dtmax和心率迅速下降,缺血2分钟后无法检测到。接触位点的数量在缺血1分钟初始增加后,缺血10分钟时降至最低。15分钟的缺血期导致接触位点数量增多,而在缺血20分钟后又再次减少。缺血2分钟后再灌注可立即恢复功能且接触位点大量存在。再灌注15分钟后,所有数值恢复到对照值。缺血10分钟后再灌注导致接触位点数量缓慢恢复,缺血15分钟后再灌注时接触位点数量仍然很低。我们可以得出结论,缺血超过15分钟后线粒体失去形成接触位点的能力,这可能是不可逆损伤的首个迹象。

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1
The effect of ischemia and reperfusion on mitochondrial contact sites in isolated rat hearts.缺血再灌注对离体大鼠心脏线粒体接触位点的影响。
Histol Histopathol. 1995 Apr;10(2):405-16.
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Effect of ischemic preconditioning on mitochondrial oxidative phosphorylation and high energy phosphates in rat hearts.缺血预处理对大鼠心脏线粒体氧化磷酸化及高能磷酸盐的影响。
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Reversible blockade of electron transport during ischemia protects mitochondria and decreases myocardial injury following reperfusion.缺血期间电子传递的可逆性阻断可保护线粒体并减少再灌注后的心肌损伤。
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Protective effects of the potent Na/H exchange inhibitor methylisobutyl amiloride against post-ischemic contractile dysfunction in rat and guinea-pig hearts.强效钠/氢交换抑制剂甲基异丁基氨氯吡脒对大鼠和豚鼠心脏缺血后收缩功能障碍的保护作用。
J Mol Cell Cardiol. 1993 Aug;25(8):959-71. doi: 10.1006/jmcc.1993.1108.

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