SODIUM RETENTION AND HEPATIC-FUNCTION FOLLOWING PARTIAL PORTAL-VEIN LIGATION IN THE RAT

Recent studies have suggested that the development of sodium retention in experimental cirrhosis in the rat occurs when hepatic function, me asured by the aminopyrine breath test, decreases below a critical thre shold. The present study evaluated the relationship between renal sodi um handling and hepatic function and determined whether sodium retenti on occurs following partial portal vein ligation. Sodium balance, urin e volume, creatinine clearance and the aminopyrine rate constant of el imination, on a constant sodium intake, were evaluated daily, from 1 d ay before surgery to 5 days after surgery, in both sham-operated (n = 6) and partially portal vein-ligated rats (n = 14). In the partially p ortal vein-ligated group, sodium retention occurred in 9 rats between 1 and 4 days after surgery, accompanied by a 45% reduction in the amin opyrine rate constant of elimination. Spontaneous natriuresis occurred within 5 days after surgery, and was associated with an increase in t he aminopyrine rate constant of elimination from 0.94 +/- 0.07 x 10(-2 ) min-1 on the last day of sodium retention to 1.36 +/- 0.06 x 10(-2) min-1 on the day of diuresis (P < 0.05). In contrast, creatinine clear ance did not change throughout the study. There was a negative curvili near association between sodium balance and the aminopyrine rate const ant of elimination (r = 0.70, P < 0.001). In the five rats without sod ium retention, there was no change in the aminopyrine rate constant of elimination and creatinine clearance over the 5 days. In another grou p of rats, measurement of portal pressure revealed similar elevations in the sodium-retaining, non-sodium-retaining, and natriuresis groups, arguing against a role for portal hypertension in initiating sodium r etention. This study suggests that the onset of sodium retention and s pontaneous natriuresis in this model is dependent on changes in hepati c function. The changes in renal sodium handling are probably mediated by tubular and not glomerular factors. The critical value of 1.15 +/- 0.07 x 10(-2) min-1 below which sodium retention occurs in this study , is similar to those reported in the carbon tetrachloride and bile-du ct ligation models of cirrhosis, and in the partial hepatectomy model of hepatic dysfunction. In conclusion, the concept of a critical thres hold has been extended to the partial portal vein ligation model in th e rat.