NITRIC-OXIDE INHIBITION AFTER HYPOXIA-ISCHEMIA ELEVATES PULMONARY ARTERIAL-PRESSURE AND INCREASES OXYGEN NEED

Inhibition of nitric oxide (NO) production may reduce posthypoxic-isch emic (HI) neonatal brain damage, but may also induce pulmonary hyperte nsion by inhibiting endogenous NO production in the pulmonary vascular bed. The aim of this study was to evaluate the effect of nitric oxide inhibition on pulmonary artery pressure and oxygen need after hypoxic ischemia. Severe HI was produced in 18 newborn lambs. After completio n of HI the lambs were divided into three groups of 6 animals receivin g either placebo (Cent), low dose N-omega-nitro-L-arginine (10 mg/kg i .v., NLA-10) or high dose (40 mg/kg i.v., NLA-40) to block NO producti on. Pulmonary artery pressure (P-ap), aortic pressure, blood gases, in spiratory oxygen concentration and ventilator settings were recorded b efore and 15, 60, 120 and 180 min after HI. Mean P-ap rose initially s ignificantly as compared to baseline in all groups at 15 min post-HI, decreased to normal in Cent but not in treated animals; 180 min post-H I mean P-ap was significantly higher in both treated groups as compare d to control (NLA-10: 32 mm Hg, NLA-40: 34 mm Hg, Cont: 25 mm Hg, p < 0.05 for NLA-10 and NLA-40 vs. Cont). Moreover, in both NLA-treated gr oups the oxygenation index was significantly elevated 120 and 180 min post-HI as compared to those of the Cent group. NO Oxygen need synthas e inhibition after HI causes a prolonged increase in Brain damage pulm onary artery pressure leading to a higher oxygen need.