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

Objectives. Although deuterium oxide (D₂O) has preservative property on the extracted organ, whether D₂O also protects the in situ myocardial injury remains unknown. Using cardiac microdialysis, local administration of D₂O through dialysis probe was applied in situ rat heart. We examined the effect of the D₂O on the myocardial injury induced ischemia, reperfusion, and chemical hypoxia. Methodology. We measured dialysate myoglobin levels during 30 min of coronary occlusion and reperfusion in the absence and presence of D₂O. Furthermore, to confirm the effect of D₂O on NaCN induced myocardial injury, we measured the dialysate myoglobin levels with local perfusion of NaCN in the absence and presence of D₂O. Results. 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. D₂O 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. Conclusions. D₂O might have a beneficial effect of myocardium against ischemia, reperfusion and chemical hypoxia.