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灌注延迟在离体心脏标本中会导致意外的缺血预处理。

Perfusion delay causes unintentional ischemic preconditioning in isolated heart preparation.

作者信息

Minhaz U, Koide S, Shohtsu A, Fujishima M, Nakazawa H

机构信息

First Department of Surgery Tokai University School of Medicine, Bohseidai, Kanagawa, Japan.

出版信息

Basic Res Cardiol. 1995 Sep-Oct;90(5):418-23. doi: 10.1007/BF00788504.

Abstract

This study sought to show that unintentional preconditioning can be induced in the isolated perfused heart during the preparation procedure. The following four groups were compared: hearts were placed in ice cold saline and cooled for 15 s and then mounted to the Langendorff apparatus (n = 5; cool immediate group); hearts were cooled for 60 s and mounted (n = 5; cool delay group); hearts were mounted directly to the apparatus within 15 s after the isolation without cooling (n = 5; noncool immediate group); hearts were mounted without cooling, but the mounting was delayed for 60 s after the isolation (n = 5; noncool delay group). All hearts were paced at a fixed rate of 300 bpm, and an occlusion of left coronary (LCA) for 60 min was performed, which was followed by reperfusion for another 60 min. Coronary flow (CBF), left ventricular developed pressure (LVDP), and creatine phosphokinase (CPK) release did not change among the four groups during ischemia. At the end of reperfusion the LVDP values were 70 +/- 1%, 66 +/- 2%, 62 +/- 3%, and 73 +/- 2% of preischemic values in cool immediate, cool delay, noncool immediate, and noncool delay groups, respectively. CPK values were 116 +/- 4, 121 +/- 7, 138 +/- 6, and 29 +/- 1 x 10(3) U/g myocardium, and percentage necrosis/risk areas were 24 +/- 1.0%, 21 +/- 1.7%, 38 +/- 2.6%, and 13 +/- 0.5% in cool immediate, cool delay, noncool immediate, and noncool delay groups, respectively. The noncool delay group demonstrated high LVDP, least amount of CPK release, and smallest size of necrosis. These results indicate that an unintentional preconditioning effect can be induced when the cooling procedure is not applied and perfusion is delayed.

摘要

本研究旨在表明,在制备过程中可在离体灌注心脏中诱导出非故意性预处理。比较了以下四组:将心脏置于冰冷盐水中冷却15秒,然后安装到Langendorff装置上(n = 5;即刻冷却组);将心脏冷却60秒后安装(n = 5;延迟冷却组);心脏在分离后15秒内直接安装到装置上,未进行冷却(n = 5;非冷却即刻组);心脏未冷却,但在分离后延迟60秒安装(n = 5;非冷却延迟组)。所有心脏均以300次/分钟的固定速率起搏,并对左冠状动脉(LCA)进行60分钟的闭塞,随后再灌注60分钟。在缺血期间,四组之间的冠状动脉血流量(CBF)、左心室舒张末压(LVDP)和肌酸磷酸激酶(CPK)释放均无变化。在再灌注结束时,即刻冷却组、延迟冷却组、非冷却即刻组和非冷却延迟组的LVDP值分别为缺血前值的70±1%、66±2%、62±3%和73±2%。CPK值分别为116±4、121±7、138±6和29±1×10³U/g心肌,即刻冷却组、延迟冷却组、非冷却即刻组和非冷却延迟组的坏死/危险区域百分比分别为24±1.0%、21±1.7%、38±2.6%和13±0.5%。非冷却延迟组表现出较高的LVDP、最少的CPK释放量和最小的坏死面积。这些结果表明,在不进行冷却程序且灌注延迟时可诱导出非故意性预处理效应。

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