Role of Portal and Splenic Vein Shunts and Impaired Hepatic Extraction in the Elevated Serum Bile Acids in Liver Cirrhosis

Ohkubo, Hideki; Okuda, Kunio; Iida, Satoshi; Ohnishi, Kunihiko; Ikawa, Shiro; Makino, Isao

doi:10.1016/s0016-5085(84)80022-0

Cited by 101 publications

(40 citation statements)

References 12 publications

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“…Whereas models of prehepatic portal hypertension, such as partial portal vein ligation in the rat, are characterized by a maximal portal-systemic shunting (above 90%) (1-4), carbon tetrachloride-induced cirrhosis in the rat is usually associated with low degrees of portal-systemic shunting, ranging from 0.2 to 30% in several studies (5-7). In contrast, dogs with portal hypertension due to secondary biliary cirrhosis may have marked degrees of portal-systemic shunting (mean values: 49%) (20), and the same appears to happen in man with alcoholic cirrhosis, in whom the extent of spontaneous portal-systemic shunting may be as high as 80% (21)(22)(23). As already mentioned, rats with carbon tetrachloride-induced cirrhosis appear to be the only portal h-ypertensive model with a low degree of spontaneous portal-systemic shunting (5-7).…”

Section: Discussionmentioning

confidence: 83%

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: Influence of the extent of portal-systemic shunting

et al. 1989

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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 After baseline measurements of portal pressure and arterial pressure, 15 ml per kg of blood were withdrawn at a rate of 0.3 ml per min and reinfused 15 min later.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)

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Section: Discussionmentioning

confidence: 83%

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: Influence of the extent of portal-systemic shunting

et al. 1989

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“…Bile salts have low MW and would pass freely into A F if they were not bound to circulating proteins and lipoproteins. Therefore, concentrations of BA in the ascites fluid of cirrhotics depend either on the unbound fraction of circulating BA [27], which contains poorly hydrophobic BA such as cholic acid [8], or on the transudation ofproteins into AF. The bile acid pattern differs largely in plasma and AF; cholic acid is the most represented bile acid in AF, whereas chenodeoxycholic acid has an opposite behaviour.…”

Section: Bile Saltsmentioning

confidence: 99%

Composition of ascitic fluid in liver cirrhosis: bile acid and lipid content

Tata¹,

Panini²,

Pellati³

et al. 1993

Eur J Clin Investigation

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Abstract. The concentrations of lipids, bile acids and proteins were evaluated in the ascitic fluid and plasma of 23 cirrhotics. Ascitic fluid density was highly correlated with its protein content, represented mostly by low molecular weight proteins. The ratio of plasma to ascitic fluid concentrations of nine examined proteins increased with molecular weight, indicating a selective ultrafiltration of the peritoneal transudate. Low density lipoproteins in ascitic fluid had modified electrophoretic mobility. Total cholesterol had a higher plasma to ascitic fluid ratio than high density lipoprotein cholesterol, whereas bile acids and proteins had similar plasma to ascitic fluid ratios. Indeed, bile acids strongly bind to circulating albumin: consequently ascitic fluid contains more cholic acid (less hydrophobic) than other bile acids. Analysis of both plasma and ascitic fluid composition in cirrhotics provides useful information on processes regulating passage of blood components into the peritoneal cavity.

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“…Bile salts are actively secreted and extracted by the liver, and plasma concentrations of bile salts are elevated in cirrhosis (4, 5). Furthermore, a strong correlation exists between increased plasma levels of bile salts and the extent of portosystemic shunting in patients with portal hypertension (6). Bile salts have physiological vasoactive properties; they have been shown to mediate postprandial intestinal hyperemia (7).…”

mentioning

confidence: 99%

Vasoactive effects of bile salts in cirrhotic rats: In vivo and in vitro studies,

Pak¹

1993

Hepatology

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To clarify a possible pathogenic role for bile salts in the hyperdynamic circulation of cirrhosis, we studied the vasoactive effects of three different bile salts-tauroursodeoxycholic acid, taurochenodeoxycholic acid and taurodeoxycholic acid-in cirrhotic rats. Cirrhosis was induced with bile duct ligation; controls underwent sham surgery. In vivo, the bile salts were intravenously infused at one of three doses (1.2 x 10(-7), 1.2 x 10(-6) and 6.0 x 10(-5) mol x 100 gm-1 x min-1) for 5 min. Taurochenodeoxycholic acid and taurodeoxycholic acid infusions increased mesenteric arterial blood flow and conductance and induced systemic arterial hypotension, whereas tauroursodeoxycholic acid had no significant effect. At similar plasma levels of bile salts, the responses in cirrhotic rats were attenuated compared with those of controls. In vitro, isolated rings of superior mesenteric and carotid arteries and portal vein were precontracted with phenylephrine; then dilatory responses to cumulative doses of bile salts (10(-6) to 10(-3) mol/L) were measured. In all three vessels, taurodeoxycholic acid produced stronger dilatory effects than did taurochenodeoxycholic acid, whereas tauroursodeoxycholic acid showed no significant effect. Vessels from cirrhotic and control rats did not differ in degree of response. These results indicate that bile salts are directly vasoactive and can induce splanchnic vasodilation at the pathophysiological plasma levels seen in cirrhosis. Bile salts may be involved in the pathogenesis of splanchnic hyperemia and hyperdynamic circulation in cirrhosis.

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Role of Portal and Splenic Vein Shunts and Impaired Hepatic Extraction in the Elevated Serum Bile Acids in Liver Cirrhosis

Cited by 101 publications

References 12 publications

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: Influence of the extent of portal-systemic shunting

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: Influence of the extent of portal-systemic shunting

Composition of ascitic fluid in liver cirrhosis: bile acid and lipid content

Vasoactive effects of bile salts in cirrhotic rats: In vivo and in vitro studies,

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