This study was carried out to elucidate the effects of nitric oxide synthase(NOS) inhibitor, NG-monomethyl-L-arginine(L-NMMA) and nitric oxide precursor, L-arginine(L-Arg) on cerebral hemodynamics and energy metabolism during reoxygenation-reperfusion(RR) after hypoxiaischemia( HI) in newborn piglets.

Twenty-eight newborn piglets were divided into 4 groups; Sham normal control(NC), experimental control(EC), L-NMMA(HI & RR with L-NMMA), and L-Arg(HI & RR with L-Arg) groups. HI was induced by occlusion of bilateral common carotid arteries and simultaneously breathing with 8 percent oxygen for 30 mins, and followed RR by release of carotid occlusion and normoxic ventilation for one hour. All groups were monitored with cerebral hemodynamics and cytochrome aa₃ (Cyt aa3) using near infrared spectroscopy(NIRS). Na⁺, K⁺-ATPase activity, lipid peroxidation products, and tissue high energy phosphate levels were determined biochemically in the cerebral cortex.

In experimental groups, mean arterial blood pressure, PaO₂, and pH decreased, and base excess and blood lactate level increased after HI compared to NC group( P <0.05). These variables subsequently returned to baseline after RR except pH. There were no differences among the experimental groups. In NIRS, oxidized hemoglobin(HbO₂) decreased and hemoglobin(Hb) increased during HI( P <0.05) but returned to base line immediately after RR; 40 min after RR, the HbO2 had decreased significantly compared to NC group( P <0.05). Changes of Cyt aa₃ decreased significantly compared to NC after HI and recovered at the end of the experiment. Significantly reduced cerebral cortical cell membrane Na⁺, K⁺-ATPase activity and increased lipid peroxidation products( P <0.05) were not improved with L-NMMA or L-Arg.

These findings suggest that NO is not involved in the mechanism of HI and RR brain damage during the early acute phase of RR.