This study was undertaken to assess splanchnic blood flow in rats with portal hypertension induced by portal vein stenosis. Splanchnic blood flow, estimated by the microsphere method, was significantly higher in portal hypertensive rats than in sham-operated rats: 26.5 +/- 3.9 (mean +/- SD) and 17.5 +/- 3.3 ml/min, respectively (P less than 0.001). Hepatic blood flow, estimated by the clearance method, was significantly lower in portal hypertensive rats than in sham-operated rats: 12.7 +/- 1.1 and 17.3 +/- 2.8 ml/min, respectively (P less than 0.001). It is concluded that splanchnic blood flow is increased in rats with portal hypertension and that hepatic blood flow is different from splanchnic blood flow in these portal hypertensive rats. It is hypothesized that splanchnic blood flow may also be increased in patients with portal hypertension.
Splanchnic organ blood flow and cardiac output were measured by the microsphere method in fasted rats with prehepatic portal hypertension due to portal vein stenosis, in rats with intrahepatic portal hypertension due to bile duct ligation, and in unoperated normal rats. Portal venous pressure was higher in both groups of portal hypertensive rats than in normal rats. Cardiac output was significantly higher in portal hypertensive rats than in normal rats. In rats with portal vein stenosis, splanchnic blood flow was higher than in controls. This increase was caused by increased perfusion of all organs drained by the portal vein, and by increased hepatic arterial blood flow. In rats with bile duct ligation, splanchnic blood flow was not significantly higher than in normal rats: haemoperfusion of all organs contributing to the portal circulation decreased, whereas hepatic arterial blood flow increased. As cardiac output rose similarly, the differences observed between the two types of portal hypertension depend mainly on the difference in distribution of flow within the splanchnic bed.
1. The effects of propranolol on heart rate, arterial pressure, portal venous pressure and fractional hepatic blood flow were studied in rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats. The effect of propranolol on cardiac output was also studied in normal rats. 2. In rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats, propranolol decreased heart rate and portal venous pressure significantly and did not alter arterial pressure. Propranolol decreased fractional hepatic blood flow significantly in rats with hepatic artery ligature, but did not change hepatic blood flow in rats with portal vein stenosis or in sham-operated rats. 3. We conclude therefore that: (a) propranolol decreases portal venous pressure in rats; (b) this decrease in portal venous pressure results in a reduction in portal blood flow which is related, in part, to a reduction in cardiac output; (c) propranolol does not alter hepatic blood flow in normal rats or in rats with portal hypertension.
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