RENAL-FUNCTION AND OXYGEN-CONSUMPTION DURING BACTEREMIA AND ENDOTOXEMIA IN RATS

Background. The hypothesis that renal failure during septic shock may occur as a result of hypoxia-related cell dysfunction was investigated in two rat models of distributive shock. Methods. Pentobarbitone-anae sthetized rats received either a bolus (1 ml) of living Escherichia co li bacteria (hospital-acquired strain, 1 x 10(9) CFU/ml: BA-group, n = 7), or a 1-h infusion of endotoxin (E. coli O127.B8: 8 mg/kg; ET-grou p, n=7), or saline to serve as time matched controls (C-group, n=7). R esults. Urine flow in the BA-and ET-group reached a nadir at 1 h, but thereafter increased and reached values higher than control at 3 h. At this time point, renal oxygen delivery had decreased, in the BA-group mainly due to a fall in arterial oxygen content and in the ET-group t o a fall in renal plasma flow (clearance of I-131-hippurate). However, renal oxygen extraction had significantly increased, by 31% in the BA and by 59% in the ET group, while renal oxygen consumption remained t he same. Net tubular sodium reabsorption had decreased by 55% in the B A and by 25% in the ET group, due to a fall in glomerular filtration r ate (clearance of creatinine). Hence, an excess oxygen consumption was found which was caused neither by an increased renal glucose release nor by the presence of an increased number of leukocytes stuck in the glomeruli. Renal tubular cells showed normal morphology. An indication that proximal tubular function in the BA and ET group remained largel y intact were normal ATP levels? absence of urinary glucose, and a nor mal fractional excretion of sodium. However, since urine flow had incr eased in shocked rats at 3 h, water appeared selectively lost. Conclus ions. Our data indicate that in rat models of septic shock renal failu re is not caused by cortical hypoxia or a shortage of cellular energy supply.