THE EFFECTS OF RYANODINE ON CALCIUM-UPTAKE BY THE SARCOPLASMIC-RETICULUM OF ISCHEMIC AND REPERFUSED RAT MYOCARDIUM

The effects of ischemia and reperfusion on sarcoplasmic reticulum (SR) calcium uptake were measured in crude heart homogenates of rats and w ere compared to published results for rabbit hearts. Isolated rat hear ts (n = 5 in each group) were Langendorff-perfused at 37 degrees C and were either kept normally perfused (control group), or submitted to 1 5 min normothermic ischemia (ischemic group), or reperfused for 10 min after 15 min ischemia (reperfused group). Mechanical function recover ed to 50-60% of control after 10 min reperfusion following ischemia. C a uptake (control V-max: 23.0 +/- 2.20 nmol.min(-1).mg of protein(-1)) decreased during ischemia (V-max: 15.7 +/- 1.60 nmol.min(-1).mg(-1)) but recovered to control level on reperfusion (V-max: 20.8 +/- 2.02 nm ol.min(-1).mg(-1)). An increased Ca uptake was obtained when the measu rements were carried out in the presence of ryanodine (430 mu M) to bl ock Ca leakage through SR Ca-release channels. The relative magnitude of ryanodine effect in the ischemic myocardium (increase: 77.2 +/- 18. 20%) was more marked than in control (32.0 +/- 8.22%) or reperfused my ocardium (39.0 +/- 10.66%). This result is different from that of rabb it myocardium where similar ryanodine effect is present in all groups (56.7 +/- 13.76%, 50.0 +/- 13.56% and 54.2 +/- 6.88% in control, ische mic and reperfused hearts, respectively) and suggests that a component of cytosolic Ca overload via SR Ca-release channels is present during ischemia in rat, but not in rabbit myocardium.