[Effects of endotoxinemia on renal and intrarenal hemodynamics of rats with or without portacaval anastomosis].

Renal dysfunction in patients with cirrhosis of the liver is frequent especially in connection with endotoxaemia. Renal and intrarenal haemodynamics were investigated, therefore, in normal rats with or without portacaval anastomosis (PCA) by means of the cardiac output (CO) fractionation technique using microspheres. The intrarenal blood distribution was estimated after anatomical separation of renal cortex and medulla. In normal rats the total renal fraction of CO was 22.5 +/- 7.2%, and the renal medulla fraction 0.8 +/- 0.4% of CO. After a single injection of E. coli-endotoxin (1.5 mg/kg b.w.) the animals developed a high-cardiac-output state, the mean arterial pressure decreased from 110 +/- 15 mm Hg to 81 +/- 6 mm Hg. Renal fraction of CO was unaltered but the blood flow through the kidney was increased due to the high CO. The blood flow of the medulla increased five to tenfold of control values whereas renal cortical blood flow decreased. During the first eight hours after endotoxin administration the animals developed polyuria with a decrease of urine osmolality. Comparable systemic and renal haemodynamics were present in untreated PCA-rats, in which endotoxaemia was present spontaneously (Limulus Gelation Test). Additional endotoxin administration in these animals caused severe shock syndrome with a decrease in total renal perfusion and a further decrease in renal cortical blood flow. Endotoxin administration in normal rats caused minimal morphological alterations in the kidneys which were comparable with those found in PCA-rats. Endotoxin administration in PCA-rats however leads to severe damage of the kidney with fibrin deposits in the glomerula and acute tubular necroses. The haemodynamic, functional and morphological changes caused by endotoxin in the experiments are observed in principle in patients with cirrhosis of the liver too. This indicates that endotoxin should be taken into considerations concerning the pathogenesis of renal failure in patients with cirrhosis of the liver.