THE EFFECT OF NITRIC-OXIDE SYNTHASE INHIBITOR ON REPERFUSION INJURY OF THE BRAIN UNDER HYPOTHERMIC CIRCULATORY ARREST

Objective: The objective of this study was to investigate the protecti ve effects of nitric oxide synthase inhibitor, N-G-nitro-L-arginine me thyl ester hydrochloride, on reperfusion injury of the brain under hyp othermic circulatory arrest. Methods: After cardiopulmonary bypass was established using 12 piglets each weighing about 30 kg, the animals w ere cooled to a brain temperature of 20 degrees C and circulatory arre st was performed for 90 minutes followed by reperfusion for 120 minute s. The level of nitric oxide within the brain was measured with a need le electrode inserted into the brain. In the treatment group, N-G-nitr o-L-arginine methyl ester hydrochloride was administered with an intra venous injection of 1.5 mg/kg at the onset of the reperfusion followed by a 60-minute continuous venous infusion of 1.5 mg/kg/hr. Results: I n the control group, nitric oxide levels within the brain increased no t during ischemia but during reperfusion, and the level after 120 minu tes of reperfusion increased significantly compared with that of befor e circulatory arrest. But in the treatment group, N-G-nitro-L-arginine methyl ester hydrochloride administered at the onset of reperfusion i nhibited nitric oxide production during reperfusion, A significant dif ference was observed between the groups regarding the nitric oxide lev el after 120 minutes of reperfusion, Regarding cerebral blood flow, ex cess lactate, and cerebral tissue water content, no significant differ ence was observed between the groups. However, recovery of somatosenso ry evoked potential after 120 minutes of reperfusion was detected in a ll six animals in the treatment group, but none in the control group ( p = 0.001). Conclusion: These data suggest that N-G-nitro-L-arginine m ethyl ester hydrochloride protects the brain against reperfusion injur y under hypothermic circulatory arrest.