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Myocardial heat shock protein changes in the failing heart following coronary artery ligation.

作者信息

Tanonaka Kouichi, Toga Wakako, Yoshida Hiroyuki, Takeo Satoshi

机构信息

Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Tokyo, Japan.

出版信息

Heart Lung Circ. 2003;12(1):60-5. doi: 10.1046/j.1444-2892.2003.00139.x.

Abstract

BACKGROUND

Production of several heat shock proteins (Hsp) is enhanced after exposure to stress. There is little information concerning changes in myocardial Hsp under pathophysiological conditions. The aim of this study was to determine alterations in Hsp content in the viable left ventricular myocardium during the development of heart failure following coronary artery ligation (CAL).

METHODS

Myocardial infarction was produced by CAL of Wistar rats. One and eight weeks after the operation, haemodynamic parameters of rats with CAL were determined and then expression of Hsp27, Hsp60 and Hsp72 was measured by western blotting.

RESULTS

Animals showed a decrease in cardiac output and an increase in left ventricular end-diastolic pressure, symptoms of chronic heart failure (CHF), 8 weeks after CAL. Myocardial Hsp27 and Hsp72 at 1 week after CAL significantly increased, whereas expression of both proteins at 8 weeks was similar to that in rats which underwent a sham operation (without coronary artery ligation). In contrast, Hsp60 at 8 weeks, but not at 1 week, significantly increased in the sham rats.

CONCLUSIONS

Diverse changes in myocardial Hsp occurred during the development of CHF.

摘要

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