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Elsewhere reviews. Nitric oxide and hyperdynamic circulation in portal hypertension
Author(s) -
Häussinger Dieter
Publication year - 1992
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840160438
Subject(s) - hyperdynamic circulation , medicine , portal hypertension , vascular resistance , portal venous pressure , cardiac output , splanchnic , nitric oxide , splanchnic circulation , omega n methylarginine , cardiology , blood pressure , hemodynamics , anesthesia , nitric oxide synthase , cirrhosis
1 The effects of inhibiting endogenous nitric oxide (NO) synthesis with N G ‐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 inflow (PVI) and portal pressure, as compared to control non‐ligated rats. 3 L ‐NMAA (6.25 and 50 mg kg −1 , i.v.) dosedependently increased MAP, reduced cardiac output and PVI, and increased peripheral and splanchnic vascular resistance. With L ‐NMMA (50 mg kg −1 ), 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 these 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 (50 mg kg −1 ). 5 These effects of L ‐NMMA (50 mg kg −1 ) were inhibited by prior administration of L ‐arginine (300 mg kg −1 , i.v.). 6 These findings indicate that the chronic hyperdynamic circulatory characteristics following portal vein stenosis can be attenuated by L ‐NMMA. Thus, the excessive formation of endogenous NO may be implicated in the pathogenesis of the haemodynamic disturbances and splanchnic vasodilatation associated with chronic portal hypertension.