Elsewhere reviews. Nitric oxide and hyperdynamic circulation in portal hypertension

✍ Scribed by Dieter Häussinger

• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: English
• Weight: 268 KB
• Volume: 16
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840160438

✦ Synopsis

The effects of inhibiting endogenous nitric oxide (NO) synthesis with W-monomethyl-L-arginine (L-NMMA) on the systemic and splanchnic circulation have been investigated in rats with experimental chronic portal hypertension, anaesthetized with ketamine.

2 Portal hypertension was induced by partial portal vein ligation, 2 weeks prior to study. This procedure induced a reduction in systemic arterial blood pressure (MAP), an increase in cardiac output as measured by radiolabelled microspheres, a reduction in peripheral and splanchnic vascular resistance and an increased portal venous M o w (PVI) and portal preesure, as compared to control non-ligated rats. 3 L-NMAA (6.25 and 50 mg kg-', i.v.) dosedependently increased MAP, reduced cardiac output and PVI, and increased peripheral and splanchnic vascular resistance. With L-NMMA (50 mg kg-'), PVI and the vascular resistances returned to values comparable to those determined in control non-ligated anaesthetized rats under resting conditions. 4 Porto-collateral resistance was also increased by thew doses of L-NMMA, whereas portal pressure was unchanged. The increase in renal blood flow and decrease in renal vascular resistance also seen in portal-hypertensive rats was reversed by L-NMMA (SO 5 These effects of L-NMMA (60 mg kg-') were inhibited by prior administration of L-arginine (300 mg kg-', i.v.1. 6 These findings indicate that the chronic hyperdynamic circulatory characteristics following portal vein stenosis can be attenuated by L-NMMA. Thus, the excemive formation of endogenous NO may be implicated in the pathogenesis of the haemodynamic distur- bances and splanchnic vasodilatation associated with chronic portal hypertension. mg kgl).