Effect of Ischemic Preconditioning on Myocardial Oxygen Consumption During Ischemia

Ischemic preconditioning (IPC) in the heart may reduce myocardial energy demand. The present study was undertaken to examine changes in myocardial oxygen consumption (MV 2) during ischemia by IPC in Langendorff perfused rat hearts. We assessed MV 2during ischemia from the measurement of mitochondrial cyt. aa3redox state by a two-wavelength reflectance spectrophotometry where T1/2, the time from the onset of ischemia to the point for half reduction of cyt. aa3, was assumed to represent MV 2. The heart was preconditioned by three cycles of 5 min ischemia plus 5 min reperfusion and then subjected to 30 min global ischemia followed by reperfusion for 30 min. The T1/2was significantly longer in the preconditioned heart (30±6 s,n=10) than the control heart (14±5 s,n=9,P<0.001), indicating a reduction of MV 2during ischemic period by IPC. The prolongation of T1/2was evident after only one IPC episode. When the heart was perfused with high K+solution to abolish MV 2for contractions, we still found the prolongation of T1/2in the preconditioned heart (116±12 s,n=6) compared to the control heart (86±10 s,n=6,P<0.01), suggesting that decrease in contractile activity may be, in part but not completely, responsible for the reduction of MV 2. In contrast, the prolongation of T1/2was completely abolished by administration of a NO synthase inhibitor Nω-nitro- -arginine in the high K+arrested heart, demonstrating involvement of NO in the reduction of MV 2, presumably by suppression of mitochondrial respiratory chain. In conclusion, IPC reduces MV 2during ischemia. The reduction of MV 2in the preconditioned heart may be accounted for by decreased contractile activity and by depression of respiratory chain by NO.