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 were compared to published results for rabbit hearts. Isolated rat hearts (n = 5 in each group) were Langendorff-perfused at 37 degrees C and were either kept normally perfused (control group), or submitted to 15 min normothermic ischemia (ischemic group), or reperfused for 10 min after 15 min ischemia (reperfused group). Mechanical function recovered to 50-60% of control after 10 min reperfusion following ischemia. Ca 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 nmol.min(-1).mg(-1)). An increased Ca uptake was obtained when the measurements were carried out in the presence of ryanodine (430 mu M) to block 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 myocardium (39.0 +/- 10.66%). This result is different from that of rabbit 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, ischemic 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.