Isoflurane attenuates myoglobin release during ischemic and/or reperfusion periods.

Abstract

Recently, we have developed cardiac microdialysis for detection of protein leakage from the injured myocardium. We examined whether the exposures to isoflurane would exert a beneficial effect on myocardial injury caused by ischemia or reperfusion. A dialysis probe was implanted into the left ventricle free wall in the rabbits. The dialysate myoglobin level served as an index of myocardial interstitial myoglobin levels. Rabbits were randomly assigned to one of three groups: (1) without exposure to isoflurane (vehicle, n=6), (2) inhale 1 MAC isoflurane once for 30 min (ISO30-1, n=6), and (3) twice for 30 min (ISO30-2, n=6). All rabbits underwent 30 min of coronary occlusion and 60 min of reperfusion. To determine whether the isoflurane induced myocardial protection against chemical hypoxia, sodium cyanide (30 mM) was administered and dialysate myoglobin levels were measured with (n=6) and without pre-exposure to isoflurane twice for 30 min (n=6). In all three groups dialysate myoglobin levels were increased by coronary occlusion and furthermore augmented by reperfusion. In comparison with the vehicle group, the ISO30-1 group suppressed only the increase in the dialysate myoglobin level during reperfusion. The ISO30-2 group suppressed during both the ischemic and reperfusion periods. Cyanide induced increases in dialysate myoglobin levels. These increments in dialysate myoglobin levels were suppressed by repeated exposure to isoflurane. Repeated exposure to isoflurane suppressed myocardial myoglobin release caused by both ischemia and reperfusion injury. Isoflurane may provide protection against myocardial ischemia/reperfusion and hypoxic injuries.