Mechanisms responsible for renal hemodynamic alterations were studied in jaundiced (by bile-duct ligation) rabbits (BDL) 10 days after ligation of the biliary tract, in comparison with sham-operated rabbits (SO). Arterial hematocrit, plasma volume, blood pressure, abdominal inferior vena cava pressure, and heart rate were not significantly different between the BDL and SO groups. Cardiac output in BDL rabbits decreased to approximately 73% of the value for SO rabbits. Renal blood flow and GFR were reduced to 64 and 61%, respectively. Reductions in blood pressure and renal blood flow, caused by bleeding (8 ml/kg of body wt), were more marked in the BDL group than they were in the SO group. In the BDL group, the recovery of blood pressure following blood infusion was slower and the mortality was higher, There was no significant increase in the renovascular sensitivity to exogenous noradrenaline or angiotensin II in the BDL group. The findings indicate that the early stage of obstructive jaundice in rabbits was characterized by altered renal perfusion partly due to reduced cardiac output and by incrased liability to hemorrhagic hypotension.

The role of renal hemodynamic alterations in the curtailment of renal function was studied in rabbits with uranyl acetate-induced acute renal failure. The day following the i.v. injection of uranyl acetate (2 mg/kg of body wt), renal blood flow (RBF) and clearance of creatinine (Ccr) decreased to approximately 60 and 20% of controls, respectively. Intracortical fractional flow distribution, estimated by radioactive microsphere method, did not change. The extraction ratio of para-aminohippurate (EPAH) decreased and the renal extraction of sodium (CNa/Ccr) increased, with minimal structural change in the kidney. Urine output increased to two to three times that of the control. After three days oliguria appeared despite complete recovery of RBF. The zonal flow redistributed toward the deep cortex. CCr and EPAH reached their minimums, concomitantly with tubular necrosis and intratubular casts. After seven days animals could be divided into the oliguric and diuretic groups. CCr and EPAH were higher in the diuretic group, while there was no significant difference in RBF and the flow distribution between groups. Regeneration of damagee tubular cells was found in the diuretic group but not in the oliguric group. The findings suggest the minor roles of RBF and the intracortical flow distribution, and a fundamental role of back leakage of filtrate across damaged tubular epithelium in the maintenance of reduced CCR and urine output during the oliguric stage in rabbits with uranyl acetate-induced renal failure.

Renal handling of salt and water in the early stage of obstructive jaundice was studied in rabbits 10 days after the ligation of the common bile duct (BDL). Sham-operated (SO) animals served as controls. No sodium retention was found in BDL rabbits, despite reduced renal perfusion and elevated plasma aldosterone level. A redistribution of intrarenal blood flow was not found. The filtration fraction did not change. A saline load resulted in decreases in arterial hematocrit and total serum proteins, and increases in urine output, urinary sodium excretion and osmolal clearance. Blood pressure, glomerular filtration rate (GFR), RPF, the filtration fraction and the intrarenal flow distribution were not significantly affected by the saline load. No significant difference was found in the natriuretic response to the saline load between the BDL and SO groups. After 60 h of water deprivation, there was no significant difference in urine-to-plasma osmolality ratios or renal tissue fluid osmolality between the BDL and SO animals. The findings indicate that renal handling of salt and water was well maintained in the early phase of obstructive jaundice in rabbits. The data also suggest the critical role of the redistribution of intrarenal blood flow rather than of GFR or aldosterone in determining sodium retention in obstructive jaundice.

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