Regional variation in rat cardiac myosin isoenzymes and ATPase activity after infarction

Three and 11 wk after coronary artery ligation in rats, the right and left ventricular free wall, septum, and papillary muscles from infarcted and sham-operated hearts were analyzed to determine whether regional variability existed in cardiac actomyosin adenosine triphosphate (ATPase) activity and myosin isoenzymes. Infarction produced a 74% greater right ventricular mass and 19% greater septal mass compared with sham-operated hearts at 3 wk. There was no additional increase in cardiac mass associated with infarction from 3 to 11 wk above that expected for normal growth. Actomyosin ATPase activity and the percent V1 myosin heavy-chain isoenzyme decreased significantly in all regions of the infarcted heart by 3 wk. In addition, the left ventricular and papillary muscle of infarcted hearts exhibited a decrease in percent V1 myosin of 18 and 35%, respectively, compared with the right ventricular free wall and septum. These differences persisted at 11 wk, although no further depression of actomyosin ATPase activity or shift in myosin isoenzyme distribution were observed over the 8-wk period. These results demonstrate that myocardial infarction induces a shift in the myosin isoenzyme distribution and depression in actomyosin ATPase activity of surviving cardiac tissue. Regional variability in myosin isoenzymes is evident by 3 wk, but additional adaptation in cardiac mass and myosin biochemistry do not occur beyond this time.