热休克蛋白的诱导可增强长时间心脏停搏后心肌和内皮功能的恢复。

Induction of heat-shock proteins enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest.

作者信息

Amrani M, Corbett J, Allen N J, O'Shea J, Boateng S Y, May A J, Dunn M J, Yacoub M H

机构信息

Cardiothoracic Surgery Department, National Heart and Lung Institute, London, England.

出版信息

Ann Thorac Surg. 1994 Jan;57(1):157-60. doi: 10.1016/0003-4975(94)90385-9.

DOI:10.1016/0003-4975(94)90385-9

PMID:8279883

Abstract

The aim of this study was to investigate the role of heat-shock proteins after heat-shock stress on the post-ischemic recovery of cardiac mechanical and endothelial function following a prolonged cardiac arrest. Isolated working rat hearts were subjected to a cardioplegic arrest for 4 hours at 4 degrees C. Three groups (n = 8 in each) were studied: (1) control, (2) sham-treated, and (3) heat-shocked rats. Postischemic recovery of cardiac output and endothelial function (as percent of preischemic control values) was 57.8% +/- 2.8% and 20.8% +/- 3.9% in group 1, 50.9% +/- 4.0% and 26.3% +/- 5.9% in group 2, and 74.0% +/- 2.4% and 51.2% +/- 8.0% in group 3, respectively. Both postischemic myocardial and endothelial function were improved by heat stress.

摘要

本研究旨在探讨热休克应激后热休克蛋白对长时间心脏骤停后心脏机械功能和内皮功能缺血后恢复的作用。将离体工作大鼠心脏在4℃下进行心脏停搏4小时。研究了三组（每组n = 8）：（1）对照组，（2）假处理组，（3）热休克大鼠组。第1组心脏输出量和内皮功能的缺血后恢复（相对于缺血前对照值的百分比）分别为57.8%±2.8%和20.8%±3.9%，第2组为50.9%±4.0%和26.3%±5.9%，第3组为74.0%±2.4%和51.2%±8.0%。热应激改善了缺血后的心肌和内皮功能。