Effects of somatostatin on splanchnic hemodynamics and plasma glucagon in portal hypertensive rats

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Abstract
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 .mu.g/kg body wt during 30 min preceded by a bolus injection of 15 .mu.g/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 reduction 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, althoguh these changes were of lesser magnitude than in portal hypertensive rats. These results suggest that increased circulating glucagon levels in the PVL model of portal hypertension contributed to the increased portal venous inflow responsible in part for portal hypertension. In addition, results indicate that circulating glucagon levels may be an important hemodynamic factor in the regulation of the portal inflow under normal conditions.