[Myocardial protection and the sarcoplasmic reticulum--the effect of ryanodine treatment prior to cardioplegic arrest on post-ischemic functional recovery].

Sarcoplasmic reticular (SR) calcium depletion may contribute to the myocardial protection against ischemia and reperfusion-induced injury. We have, therefore, investigated the effect of ryanodine-induced SR calcium depletion on the myocardial protection when given during Langendorff perfusion before ischemia in the isolated working rat heart. Hearts (n = 6/group) from male Wistar rats were aerobically (37 degrees C) perfused (20 min) with bicarbonate buffer (the first working perfusion), and then aerobically (37 degrees C) perfused with bicarbonate buffer containing 0, 1.75 or 7.00 nmol/L of ryanodine (a Langendorff perfusion). Hearts were then aerobically (37 degrees C) perfused (20 min) with ryanodine-free bicarbonate buffer (the second working perfusion). This was followed by a 3 min infusion of St. Thomas' Hospital cardioplegic solution, and then subjected to 38 min of normothermic (37 degrees C) global ischemia and 35 min of reperfusion (15 min Langendorff, 20 min working). After the ryanodine treatment, the percent reduction in aortic flow was significantly greater in the 7.00 nmol/L ryanodine group than in the control group. The post-ischemic recoveries of aortic flow were 39.1 +/- 3.3, 32.8 +/- 5.3 and 37.3 +/- 4.4% in the 0, 1.75 and 7.00 nmol/L ryanodine groups, respectively. There was no difference in the creatine kinase leakage during Langendorff reperfusion between the ryanodine-treated groups and the control group. Thus, ryanodine decreased the cardiac function after the ryanodine treatment, indicating a reduction in SR calcium content. Ryanodine, however, failed to improve the post-ischemic functional recoveries.(ABSTRACT TRUNCATED AT 250 WORDS)