1. Systemic haemodynamics and kidney function were studied in the same dogs before and 14 days after choledochocaval anastomosis. 2. All dogs became deeply jaundiced whereas parenchymal liver function remained unchanged as assessed biochemically. 3. After choledochocaval anastomosis there was a decrease in mean arterial pressure (118 ± 18 to 98 ± 13 mmHg, P < 0·005), and total peripheral resistance (4073·8 ± 620·0 to 3327·6 ± 244·9 kPa l −1 s kg, P < 0·01), whereas mean cardiac index and plasma volume corrected for body weight did not change. 4. Despite their disturbed systemic haemodynamics the cholaemic dogs had normal mean glomerular filtration rate and renal plasma flow. Maximal ability to concentrate and dilute the urine was, however, impaired during cholaemia. 5. It is concluded that cholaemia per se cuases peripheral vasodilatation, hypotension and renal tubular dysfunction. Similar phenomena in jaundiced patients may contribute to their susceptibility to postoperative shock and acute renal failure.
1. Obstructive jaundice sensitizes the kidney to anoxic damage. To clarify further this phenomenon the effect of unilateral infusion of bile on kidney function was studied. The contralateral intact kidney served as control. 2. Intrarenal infusion of diluted bile (1:10) resulted in an ipsilateral fourfold increase in mean rate of urinary flow ( P < 0.01), threefold increase in mean fractional excretion of sodium ( P < 0.05) and more than 50% increase in mean rates of potassium excretion ( P < 0.05). Urinary flow rate and electrolyte excretion returned to baseline upon cessation of bile infusion. The mean clearances of inulin and p -aminohippurate were unchanged during intrarenal bile infusion. 3. Intrarenal infusion of isotonic taurocholate solution (20 mmol/l) mimicked the diuretic, natriuretic and kaliuretic effects of diluted bile, whereas intrarenal infusion of bilirubin did not cause any change in the excretion of electrolytes. 4. It is concluded that increase in circulating bile acids rather than hyperbilirubinaemia may alter kidney function during obstructive jaundice. Acute cholaemia may cause volume depletion by increasing urinary salt loss. This in turn may aggravate the direct nephrotoxicity of circulating bile compounds.
1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL). 2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 ± 62 vs 960 ± 58 μmol/min in the control period before CBDL ( P < 0.001). This antinatriuresis was associated with a significant rise in plasma aldosterone concentration, from 52.5 ± 5.5 pg/ml before CBDL to 177 ± 50 pg/ml after CBDL ( P < 0.02). Ascites was present in all salt-retaining CBDL dogs. 3. Bilateral adrenalectomy resulted in disappearance of ascites and in a rise in the natriuretic response to extracellular volume expansion. Urinary sodium excretion was 770 ± 124 μmol/min, a value significantly higher than in the CBDL dogs with intact adrenals ( P < 0.001). Sodium balance studies in the adrenalectomized CBDL dogs during chronic deoxycorticosterone acetate (DOCA) treatment (25 mg/day) showed that in these animals there was failure to escape from the mineralocorticoid-induced sodium retention. Glomerular filtration rate and renal plasma flow did not change during the studies. 4. The present evidence supports the thesis that sodium retention in the CBDL dog results from a dual mechanism: (a) excess of circulating aldosterone and (b) an extra-adrenal factor which prevents escape from the salt-retaining effect of mineralocorticoids, in the CBDL dogs, thereby perpetuating the antinatriuresis in these animals.