The present study investigated whether, in rats with portal hypertension due to cirrhosis of the liver induced by carbon tetrachloride, blood volume restitution following a hemorrhage produces an increase of portal pressure beyond control values, as observed in rats with prehepatic portal hypertension. Since carbon tetrachloride-induced cirrhosis caused mild portal-systemic shunting, in some of the cirrhotic rats (12 of 29 rats) portal-systemic shunting was enhanced by a transient (4 days) partial constriction of the portal vein, which was removed 1 week prior to the study. After baseline measurements of portal pressure and arterial pressure, 15 ml per kg of blood were withdrawn at a rate of 0.3 ml per min and reinfused 15 min later. After blood reinfusion, portal pressure and arterial pressure were measured again, and cardiac output, regional blood flows and portal-systemic shunting were determined using radioactive microspheres. Portal-systemic shunting was 78 +/- 11% of total blood flow in the cirrhotic rats that had temporary portal vein constriction, but only 5 +/- 2% (p less than 0.001) in those that did not. Blood volume restitution in low-portal-systemic shunting rats did not produce any significant modification in splanchnic or systemic hemodynamics. However, in rats with high portal-systemic shunting, blood volume restitution produced a significant increase in portal pressure (from 9.9 +/- 0.9 to 13.5 +/- 0.9 mmHg, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of somatostatin infusion on splanchnic and systemic hemodynamics and plasma glucagon levels were investigated in rats with portal hypertension. Forty-four male Sprague-Dawley rats were studied. Portal hypertension was induced in 26 rats by partial portal vein ligation (PVL). These rats were divided in two experimental groups to receive blindly 1) somatostatin (PVL-SMT, n = 13) at a dose of 25 micrograms/kg body wt during 30 min preceded by a bolus injection of 15 micrograms/kg body wt or 2) placebo (saline) (PVL-P, n = 13) infused at the same rate as in the previous group. The remaining 18 rats were used as normal controls and received somatostatin (n = 9) or saline infusion (n = 9). Regional blood flows and cardiac output were measured using radioactive microspheres. Arterial and portal pressures were also measured. In portal hypertensive rats somatostatin infusion produced significant reductions in the increased portal venous inflow, reductions in portal pressure, and significantly increased portal venous resistance. Reduction of portal venous inflow was due to splanchnic vasoconstriction, evidenced by increased splanchnic arteriolar resistance. No significant differences were observed in systemic hemodynamic parameters between PVL-SMT and PVL-P rats. Plasma glucagon levels were significantly reduced by somatostatin to levels similar to those observed in sham-operated rats. In sham-operated rats, somatostatin also caused significant reduction in portal venous inflow and plasma glucagon concentration, although these changes were of lesser magnitude than in portal hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The study was aimed at investigating whether increased portal venous inflow (PVI) after portocaval shunt (PCS) in the rat is the result of selective splanchnic vasodilatation or whether it is part of a generalized circulatory disturbance. Rats with PCS (n = 9) and sham-operated controls (n = 8) were studied 2 wk after surgery by measuring cardiac output (CO), PVI, and hepatic artery flow (HAF) with radioactive microspheres. Plasma glucagon (GL) was measured by radioimmunoassay. PCS rats had increased CO (46.2 +/- 2.8 vs. 28.2 +/- 1.7 ml X min-1 X 100 g-1, P less than 0.001) and reduced arterial pressure and total peripheral resistance. PVI was markedly increased (7.7 +/- 0.7 vs. 4.3 +/- 0.2 ml X min-1 X 100 g-1, P less than 0.001), but this appeared to be part of a generalized circulatory disturbance, since when PVI is expressed as percent of CO no difference is observed between PCS and sham-operated rats (17.0 +/- 1.5 vs. 15.8 +/- 1.3%, NS), indicating the absence of a preferential splanchnic vasodilatation. GL increased after PCS (548 +/- 130 vs. 156 +/- 23 pg/ml, P less than 0.005), and significant correlations were observed between GL and CO (r = 0.787, P less than 0.001) and between GL and PVI (r = 0.806, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)