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

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

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.

MeSH terms

  • Animals
  • Cardiac Output
  • Heart Arrest, Induced*
  • Heat Exhaustion / metabolism*
  • Heat-Shock Proteins / metabolism*
  • Male
  • Nitric Oxide / metabolism
  • Rats

Substances

  • Heat-Shock Proteins
  • Nitric Oxide