Evaluation of postprandial hyperemia in superior mesenteric artery and portal vein in healthy and cirrhotic humans: an operator-blind echo-Doppler study.

In an operator-blind design, we used an echo-Doppler duplex system to examine superior mesenteric artery and portal vein hemodynamics on two consecutive mornings in 12 fasting cirrhotic patients and 12 matched controls, randomized to a standardized 355 kcal mixed-liquid meal vs. water. Cross-sectional area and mean velocity were recorded from the portal vein and superior mesenteric artery at 30 min intervals, from 0 min to 150 min after ingestion. Flows were calculated. Pulsatility index, an index related to vascular resistance, was obtained for the mesenteric artery. Baseline flows did not differ between cirrhotic patients and control patients, but pulsatility index was reduced in the cirrhotic subjects. Maximal postprandial hyperemia was attained at 30 min. Cirrhotic patients showed a blunted hyperemic response to food. In normal controls, portal vein area increased significantly after the meal from 30 min to 150 min, whereas in cirrhotic patients a significant difference occurred only at 30 min. Pulsatility index in both groups was significantly reduced after eating, and this reduction persisted up to 150 min. No changes after ingestion of water were observed. Echo-Doppler was very sensitive in detecting postprandial splanchnic hemodynamic changes and differences between cirrhotic patients and normal subjects. Mesenteric artery pulsatility index was more sensitive than flow in detecting baseline hemodynamic differences. In cirrhotic patients, portal postprandial hyperemia was mainly related to the increase in mean velocity.

Na restriction blunts expansion of plasma volume and ameliorates hyperdynamic circulation in portal hypertension.

Expansion of plasma volume may be necessary for the development of the hyperdynamic circulation in portal hypertension. In experiment 1, sham portal vein-constricted (sham PVL) rats were divided into normal diet (NL diet sham) and low-sodium diet (low-Na sham) groups. Data obtained from the NL diet sham group was used as control data in studying portal hypertensive rats, which were also divided into normal diet (NL diet PVL) and sodium-restricted (low-Na PVL) groups on the day of portal vein constriction. There were no hemodynamic differences at 3 wk between sham PVL rats on the two diets. In contrast, sodium restriction in PVL rats resulted in a significant amelioration of the hyperdynamic circulation. In experiment 2, PVL rats were fed a normal diet for 10 days, followed by allocation to NL diet PVL and low-Na PVL groups. The hemodynamic effects of sodium restriction in these animals (studied at 22 and 28 days after PVL) were similar to those observed in experiment 1. A time course for amelioration of the hyperdynamic circulation in PVL rats by sodium restriction is described. Sodium restriction prevents the expansion of the plasma volume in PVL rats. Interference with plasma volume expansion blunts the development of (and can ameliorate) the hyperdynamic syndrome. Plasma volume expansion seems necessary for the development of the hyperdynamic circulation in portal hypertension.

Bile acids do not mediate the hyperdynamic circulation in portal hypertensive rats.

Portal hypertension is accompanied by hyperdynamic systemic and splanchnic circulation. Serum bile acids (BAs), which are elevated in portal hypertension and have vasodilatory properties, have been proposed as mediators of this hyperdynamic circulation. In this study, portal hypertensive rats [accomplished by partial portal vein ligation (PVL)] were gavaged with cholestyramine (PVL-CH) to decrease circulating BA levels. A control group of rats was gavaged with an inert suspension of Metamucil (PVL-ME). The following hyperdynamic parameters were found to be similar in PVL-CH and PVL-ME: mean arterial pressure (119 +/- 6 vs. 124 +/- 5 mmHg), portal pressure (13.2 +/- 0.6 vs. 14.5 +/- 0.5 mmHg), cardiac index (0.33 +/- 0.04 vs. 0.34 +/- 0.03 ml.min-1.g body wt-1), splanchnic blood flow (1.4 +/- 0.13 vs. 1.6 +/- 0.1 ml.min-1.g body wt-1), portosystemic shunting (82 +/- 8 vs. 92 +/- 3%), peripheral arteriolar resistances (344 +/- 74 vs. 387 +/- 29 mmHg.min.ml-1.g body wt), and splanchnic arteriolar resistances (75 +/- 14 vs. 72 +/- 6 mmHg.min.ml-1.g splanchnic wt; 1,471 +/- 150 vs. 1,325 +/- 120 mmHg.min.ml-1.g body wt). BA in PVL-ME (84 +/- 9 microM/l) were similar to those previously observed in untreated PVL and significantly greater than those measured in PVL-CH (25 +/- 4 microM/l; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)