Assessment of Portal and Hepatic Hemodynamics after Side-to-Side Portacaval Shunt in Patients with Cirrhosis*

Redeker, Allan G.; Kunelis, Constantine T.; Yamamoto, Shinichi; Reynolds, Telfer B.

doi:10.1172/jci105022

Cited by 22 publications

(6 citation statements)

References 6 publications

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“…Also, in patients with cirrhosis who had portacaval anastomoses without ascites, and who presumably had a decrease in intrahepatic as well as splanchnic congestion as a result of this operation, the mean plasma volume was significantly elevated (p < 0.0001). This elevation occurred even in those patients with side-to-side portacaval anastomoses, which are thought to decongest the liver maximally (35,36) (Figure 1). Those 14 patients with cirrhosis who had portacaval anastomoses proven to be patent at autopsy in four and by catheterization in one, yet who had coexisting ascites, also had an elevated mean plasma volume (51 + 3.0 ml per kg, p < 0.01) (Figure 1).…”

Section: Methodsmentioning

confidence: 99%

“…The following three possibilities occur to us: 1) The portacaval anastomosis, by decreasing hepatic blood flow, might keep the plasma volume from falling to normal. Evidence has been presented recently to show that hepatic degradation of aldosterone is dependent on liver blood flow (52)(53)(54), and it is possible that a reduction in hepatic blood flow produced by portacaval anastomosis of either the end-to-side or side-to-side variety (36) could elevate the plasma aldosterone concentration sufficiently to keep the plasma volume expanded.…”

Section: Plasma Volume In Functional Renal Failurementioning

confidence: 99%

See 1 more Smart Citation

Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure*

Lieberman¹,

Reynolds²

1967

J. Clin. Invest.

217

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Section: Methodsmentioning

confidence: 99%

Section: Plasma Volume In Functional Renal Failurementioning

confidence: 99%

Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure*

Lieberman¹,

Reynolds²

1967

J. Clin. Invest.

217

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“…Numerous studies have established the effectiveness of such a PCA in returning previously elevated sinusoidal pressures to normal (10,(18)(19)(20). Although it is known that either a combination of a cirrhotic liver and intrahepatic hypertension (7) or intrahepatic hypertension alone (21,22) are potent sodium retaining states, it is not known whether a cirrhotic liver per se will also provide a sodium retaining stimulus.…”

Section: Resultsmentioning

confidence: 99%

Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites.

Unikowsky¹,

Wexler²,

Levy³

1983

J. Clin. Invest.

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A B S T R A C T Dogs with portal cirrhosis but without portal hypertension (end-to-side portacaval anastomosis) retain sodium and expand plasma volume before ascites formation. In our study, dogs were subjected to bile duct ligation and simultaneous side-toside portacaval anastomosis (PCA) in order to create a canine model of hepatic cirrhosis without intrahepatic or portal hypertension. The effect of normalizing intrahepatic pressures in the face of venous outflow block on sodium handling was studied. 13 dogs survived the surgical procedures and were followed. Two dogs developed sodium retention and ascites at 5-6 wk (livers were cirrhotic) when the PCA spontaneously closed. 11 dogs were free of sodium retention and ascites for as long as 12 wks after surgery, while ingesting 35 meq/d of sodium. In this group glomerular filtration rate remained normal throughout the period of observation and there was no expansion of plasma volume. Nine of these dogs were then fed 85 meq/d of sodium; eight remained in sodium balance and one retained sodium and went on to develop ascites. When 10-15 mg i.m. of desoxycorticosterone acetate (DOCA) was given daily, five dogs developed sodium retention and ascites, while four escaped from DOCA. Dogs who developed ascites had either a partially occluded PCA (4/5) or a patent PCA, but with a significant portacaval pressure gradient of 9.5 cm H20

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“…His data were drawn retrospectively from studies ofhepatic blood flow after portacaval shunt (51,52) and, therefore, excluded patients who died early or had poor liver function that precluded blood flow measurement. Furthermore, the additional variable of inferior vena caval pressure was introduced by subtracting inferior vena caval pressure from the wedged hepatic venous pressure.…”

Section: Discussionmentioning

confidence: 99%

Effect of Portal Venous Blood Flow Diversion on Portal Pressure

Zimmon¹,

Kessler²

1980

J. Clin. Invest.

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A B S T R A C T To anticipate the hepatic vascular response to portacaval anastomosis, we studied portal pressure during diversion of portal blood through a temporary extracorporeal umbilical vein to saphenous vein shunt. The relationship of portal pressure to shunted flow was approximately linear. In five schistosomiasis patients (controls) portal diversion to 1,250 ml/min gave portal pressure-shunted flow curve slopes ranging from 0.13 to 0.57 cm water/100 ml per min (0.31±0.18, mean+SD). In 17 cirrhotic patients with portal hypertension a continuum of slopes was observed from within mean±2 SD of control (type A) to larger slopes (type B) indicating failure of portal pressure regulation. When portal flow was augmented by shunting from saphenous vein to portal vein, cirrhotic patients who had slopes less than mean ±2 SD ofcontrols during diversion (type A) exhibited a compliant system with small increases in portal pressure, whereas type B patients had significantly greater pressure increases. Selective investigations suggested that changes in portal pressure provoked compensatory changes in hepatic arterial blood flow that tended to maintain portal pressure at a set point. Type B patients demonstrated failure of this mechanism to varying degrees.After end-to-side portacaval shunt, seven type A cirrhotic patients maintained residual intrahepatic venous pressure unchanged from prior portal pressure, whereas six type B patients had a significant decrease. Residual intrahepatic venous pressure was measured after portacaval shunt in 40 cirrhotic patients who were followed This work was presented in part at the annual meetings of the American Association for the Study of Liver Disease,

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Assessment of Portal and Hepatic Hemodynamics after Side-to-Side Portacaval Shunt in Patients with Cirrhosis*

Cited by 22 publications

References 6 publications

Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure*

Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure*

Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites.

Effect of Portal Venous Blood Flow Diversion on Portal Pressure

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