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Am J Physiol Renal Physiol 253: F664-F671, 1987;
0363-6127/87 $5.00
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AJP - Renal Physiology, Vol 253, Issue 4 664-F671, Copyright © 1987 by American Physiological Society

ARTICLES

Hepatic denervation alters first-phase urinary sodium excretion in dogs with cirrhosis

M. Levy and M. J. Wexler
Department of Physiology, McGill University, Montreal, Quebec, Canada.

Cirrhotic dogs without intrahepatic hypertension (IHH) never retain sodium or expand plasma volume. To test the hypothesis that IHH may cause urinary sodium retention early in cirrhosis, we prepared cirrhotic dogs (chronic biliary obstruction) who underwent simultaneous hepatic denervation with end-side portacaval anastomoses. Such animals, along with appropriate controls and unanesthetized were studied by balance techniques. In the experimental group, plasma volume never increased, and sodium retention did not occur until 2 days prior to the appearance of detectable ascites. In a sham-denervated group, plasma volume increased by 10% and sodium retention occurred on the average 8.4 days prior to ascites. When the portal veins were left intact, the sham-denervated group showed the usual magnitude of plasma volume expansion observed in cirrhotic dogs (18.3%) with a 7-day delay between sodium retention and ascites appearance. Those dogs with hepatic denervation demonstrated a 9.2-day delay with 12.6% expansion of plasma volume. When ascites was mobilized with a peritoneovenous valve, and dogs were subjected to a high salt diet (130 meq/day), denervated dogs excreted the load normally, whereas sham-denervated dogs retained sodium and developed anasarca. We conclude that in cirrhotic dogs with IHH, liver denervation prevents early non-volume-related sodium retention.


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