Renal perfusion and metabolism in experimental endotoxin shock.

Abstract

Central and renal hemodynamics, renal oxygenation, renal uptake of glucose, lactate, fats, renal carnitine metabolism, arterial atrial natriuretic factor (ANF) and catecholamine release were studied in sixteen adult beagle dogs during pentobarbital anesthesia. Renal cortical oxygen tension was recorded by means of a Silastic tonometer. Twelve animals underwent acute circulatory shock induced by intravenous Escherichia coli endotoxin 0.5 mg/kg. Four control dogs received normal saline. The endotoxin infusion resulted in decreased cardiac function, renal blood flow and renal cortical PO2. The renal venous PO2 increased during the experiment. Arterial and renal venous glucose concentrations increased transiently during endotoxemia. Circulating lactate concentrations increased significantly whereas the arteriovenous lactate difference remained almost unchanged. Renal uptake of lactate and glucose were not influenced during the moderate renal hypoperfusion caused by endotoxin. Arterial free fatty acid (FFA) concentrations increased significantly 2 hours after onset of the endotoxin infusion whereas renal venous FFA levels remained rather stationary. The renal uptake of FFA increased with increasing arterial FFA concentrations. Circulating free carnitine concentrations increased significantly in endotoxin shock. Blood acyl-carnitine concentrations remained essentially unchanged. Carnitine concentrations declined significantly in endotoxic renal tissue. The arterial concentrations of ANF, epinephrine, norepinephrine and the norepinephrine metabolite 3,4-dihydroxyphenylglycol (DHPG) increased in plasma during early endotoxemia. The levels of these hormones remained very low and constant in the controls. To summarize, endotoxin injection resulted in impaired renal perfusion and oxygenation, increased uptake of free fatty acids and unchanged uptake of glucose, lactate, glycerol and triglycerides. Decreased renal carnitine concentrations were observed. Arterial plasma concentrations of ANF and catecholamines increased in endotoxin shock.