Mechanical performance of spared myocytes after myocardial infarction in rats: effects of captopril treatment.

To determine the effects of myocardial infarction-induced left ventricular failure on the mechanical characteristics of the remaining viable myocytes, coronary arterial occlusion was performed in rats, and cell function was examined 1 wk later. Moreover, to establish the mechanisms by which treatment with angiotensin-converting enzyme inhibitors ameliorates cardiac dynamics, captopril was administered immediately after surgery, and the contractile behavior of the unaffected cells was similarly analyzed 7 days later. The severe impairment in left-side pump function was found to be associated with a decrease in the velocities of myocyte shortening and relengthening and peak shortening despite a prolongation of contraction duration. In addition, a uniform property was recognized in myocytes from infarcted and noninfarcted hearts. Longer cells manifested greater velocity of shortening, whereas wider cells of identical length exhibited depressed shortening velocity. After infarction, the depression in cell contractility coupled with lateral expansion of myocytes exceeded the influence on cell mechanical behavior linked to myocyte lengthening leading to an overall decrease in contractility of the hypertrophied cells. Captopril therapy preserved, in part, the ability of myocytes to shorten and relengthen, which was accompanied by a decrease in the lateral and longitudinal expansions of these cells.