Deuterium oxide protects against myocardial injury induced by ischemia and reperfusion in rats.

. Although deuterium oxide (DO) has preservative property on the extracted organ, whether DO also protects the in situ myocardial injury remains unknown. Using cardiac microdialysis, local administration of DO through dialysis probe was applied in situ rat heart. We examined the effect of the DO on the myocardial injury induced ischemia, reperfusion, and chemical hypoxia. . We measured dialysate myoglobin levels during 30 min of coronary occlusion and reperfusion in the absence and presence of DO. Furthermore, to confirm the effect of DO on NaCN induced myocardial injury, we measured the dialysate myoglobin levels with local perfusion of NaCN in the absence and presence of DO. . The dialysate myoglobin levels increased from 177 ± 45 ng/mL at baseline to 3030 ± 1523 ng/mL during 15-30 min of coronary occlusion and further increased to 8588 ± 1684ng/mL at 0-15 min of reperfusion. The dialysate myoglobin levels with 60 min local perfusion of NaCN increased to 1214 ± 279 ng/mL. DO attenuated myocardial myoglobin release during 15-30 min of coronary occlusion and 0-30 min of reperfusion and 15-60 min of local perfusion of NaCN. . DO might have a beneficial effect of myocardium against ischemia, reperfusion and chemical hypoxia.