UNDIMINISHED MITOCHONDRIAL-FUNCTION DURING STUNNING IN RABBIT HEART AT 28-DEGREES-C

Objective: To investigate effect of brief ischemia on mitochondrial fu nction in intact myocardium, rather than in isolated mitochondria. Met hods: The mitochondrial response was characterized by the mean respons e time (t(mito)) of cardiac mitochondrial O-2 consumption to steps in heart rate. Isolated isovolumic rabbit hearts were perfused at 28 degr ees C with a constant flow of Tyrode solution containing 11 mM glucose . O-2 consumption and t(mito) were determined before ischemia and afte r 25 min of no-flow global ischemia during which hearts were either pa ced (I + P, n = 8) or unpaced (I - P, n = 8). A non-ischemic control g roup (n = 8) was also examined. Results: At 20 min reperfusion, develo ped left ventricular pressure (DLVP) after I + P was decreased to 47 /- 3% (mean +/- s.e.m.; P < 0.05) of control DLVP without significant changes in venous creatine kinase efflux, indicating contractile stunn ing. In contrast, complete contractile recovery was observed after I - P. Before ischemia, t(mito) was 11.2 +/- 0.6 and 14.9 +/- 0.7 s for h eart rate steps from 60 to 70 and from 60 to 120 beats/min, respective ly. The t(mito) was lower(P < 0.05) for the corresponding downward ste ps (10.5 +/- 0.6 and 12.4 +/- 0.6 a, respectively). An increase (P < 0 .05) in t(mito) was observed in the course of the experiment for upwar d (1.2 +/- 0.3 s) and downward steps (1.4 +/- 0.3 s), but the change w as similar after ischemia to that in time-matched controls (P > 0.05, both for I - P and I + P vs. control), Oxygen consumption, compared at fixed levels of the rate x pressure product, was unchanged after isch emia (P > 0.05, for both I - P and I + P vs. controls), suggesting und iminished efficiency of mitochondrial ATP production. Conclusions: Twe nty-five minutes ischemia does not affect mitochondrial function in ra bbit hearts at 28 degrees C, even when contractile stunning resulted. (C) 1997 Elsevier Science B.V.