Biol. Pharm. Bull. 30(1) 105—110 (2007)

kinds of sublethal stress such as heat shock, toxins, heavy metal ions, and chemicals results in the induction of heat shock proteins (Hsps). Hsps are considered to be involved in the maturation of newly synthesized proteins and in the degradation of damaged proteins, leading to cell proliferation, differentiation, adaptation to various circumstances, and protection of cells against stress-induced damage. In a previous study, we examined the beneficial roles of Hsp70 in the viable left ventricle in the pathogenesis of chronic heart failure. Hsp60 is a chaperon located in the mitochondrial matrix space under physiological conditions, and it may be involved in protein transport from the cytosol into mitochondria across the mitochondrial inner membrane. Recently, Knowlton et al. showed an increase in the Hsp60 content of the human heart at the end stage of both ischemiaand dilatation-elicited cardiomyopathies. Several investigators have reported that antibodies against Hsp60 appeared in the serum of the patients with acute coronary syndrome or hypertension. In a previous study, we showed a decrease in high-energy phosphates of the failing heart following acute myocardial infarction. These findings suggest that an increased level of myocardial Hsp60 plays some roles in the development of heart failure. Thus, in the present study, we examined the relationship between the Hsp60 content and mitochondrial function in the viable cardiac muscle after myocardial infarction. In earlier reports on our ongoing series of studies on myocardial infarction, we showed that when rats with myocardial infarction were treated for 6—10 weeks with angiotensin I-converting enzyme inhibitor (ACEI) trandolapril, there were improvements in their hemodynamics, energy metabolism, b-adrenoceptor signaling, and heat shock-induced Hsp72 production. However, the effects of long-term treatment with trandolapril on the increase in myocardial Hsp60 after myocardial infarction remain unclear. Therefore, the second purpose of the present study was to examine the effect of trandolapril on the increase in Hsp60 during the development of heart failure after myocardial infarction.