In portal hypertensive states, peripheral vasodilation leads to
sodium retention and plasma volume expansion.
N omega-nitro-L-arginine, a specific biosynthesis inhibitor of the
vasodilator nitric oxide, has been shown to acutely reverse peripheral vasodilation and the vascular hyporesponsiveness to endogenous and exogenous
vasoconstrictors observed in portal hypertensive rats. This study investigated whether
N omega-nitro-L-arginine treatment in portal hypertensive rats prevents peripheral vasodilation and therefore ameliorates plasma volume expansion and
sodium retention. For 2 days before partial portal vein
ligation or
sham operation and then continuously for 4 days after the operation, animals received either placebo (
0.9% saline) or
N omega-nitro-L-arginine (approximately 2 micrograms/kg/min) intravenously through a subcutaneously implanted Alzet osmotic pump (model 2ML1; Alza, Palo Alto, CA). In portal hypertensive rats,
N omega-nitro-L-arginine treatment significantly increased mean arterial pressure (placebo vs.
N omega-nitro-L-arginine, 123 +/- 4 vs. 150 +/- 2 mm Hg, respectively; p < 0.001) and systemic vascular resistance (3.8 +/- 0.2 vs. 5.6 +/- 0.3 mm Hg/ml/min/100 gm
body weight; p < 0.001), associated with a decrease in the cardiac index (33.5 +/- 1.0 vs. 27.0 +/- 1.1 ml/min/100 gm
body weight; p < 0.001).
N omega-nitro-L-arginine treatment also induced a decrease in plasma volume (4.6 +/- 0.1 vs. 4.1 +/- 0.1 ml/100 gm
body weight; p < 0.001) and extracellular
sodium space (39.4 +/- 0.7 vs. 37.4 +/- 0.4 ml/100 gm
body weight; p < 0.05) without changes in serum
sodium.(ABSTRACT TRUNCATED AT 250 WORDS)