The Effects of Nitric Oxide Inhibitor on Hyperdynamic Circulation in Portal Hypertensive Rats / 영남의대학술지

ABSTRACT

BACKGROUND: Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells. accounts for the biological activity of endothelium derived relaxing factor. Previous studies demonstrated that nitric oxide inhibitor. N'-Nitro-L-Arginine(NNA)diminished the hyperdynamic splanchnic and systemic circulation in portal hypertensive rats. The present study was done to determine the role of nitric oxide in the development of hyperdynamic circulations in the prehepatic portal hypertensive rat model produced by partial portal vein ligation. METHODS: The portal hypertensive rats were divided into water ingestion group and NNA ingestion group. After partial portal vein ligation. NNA ingestion group and water ingestion group received NNA, 1mg/kg/day and plain water through the mouth for 14 days, respectively. Cardiac output, mean arterial pressure, organ blood flow and porto-systemic shunting were measured by radioisotope microsphere methods. Vascular resistances were calculated by standard equation. RESULTS: There were significant decreases in mean arterial pressure, increases in cardiac output and cardiac index, and decreases in total systemic and splanchnic vascular resistance in portal hypertensive rats compared to normal control froup(p<0.01). Compared to the water ingestion group, significantly increased mean arterial pressure wit decreased cardiac output and cardiac index were dexeloped in the NNA ingestion group. Total systemic and splanchnic vascular resistance were significantly increased in the NNA ingestion group compared to water ingestion group(p<0.05). But, there was no significant difference in portal pressure between the two groups. CONCLUSION: The hemodynamic results of this study indicate that hyperdynamic circulation in prehepatic portal hypertensive rat model was attenuated by ingestion of NNA. Nitric oxide may play an important role in the development of hyperdynamic circulation with splanchnic vaodilation in chronic portal hypertension.