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.