Cardiac Sarcoplasmic Reticular Function in Rats with Chronic Heart Failure Following Myocardial Infarction

Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25–0.5 min with 10−5mCa2+(53–70%) and when preloaded with 10−6mCa2+and then exposed to 0.1–1mmcaffeine (39–87%). The results suggest that the rate of Ca2+uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+released from SR decreased due to decreased Ca2+uptake rate of SR and down-regulation of the SR Ca2+-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction.