Abstract
IntroductionSeptic renal failure is often seen in the intensive care unit but its pathogenesis is only partly understood. This study, performed in a normotensive rat model of endotoxemia, tests the hypotheses that endotoxemia impairs renal microvascular PO2 (μPO2) and oxygen consumption (VO2,ren), that endotoxemia is associated with a diminished kidney function, that fluid resuscitation can restore μPO2, VO2,ren and kidney function, and that colloids are more effective than crystalloids.MethodsMale Wistar rats received a one-hour intravenous infusion of lipopolysaccharide, followed by resuscitation with HES130/0.4 (Voluven®), HES200/0.5 (HES-STERIL® ® 6%) or Ringer's lactate. The renal μPO2 in the cortex and medulla and the renal venous PO2 were measured by a recently published phosphorescence lifetime technique.ResultsEndotoxemia induced a reduction in renal blood flow and anuria, while the renal μPO2 and VO2,ren remained relatively unchanged. Resuscitation restored renal blood flow, renal oxygen delivery and kidney function to baseline values, and was associated with oxygen redistribution showing different patterns for the different compounds used. HES200/0.5 and Ringer's lactate increased the VO2,ren, in contrast to HES130/0.4.ConclusionThe loss of kidney function during endotoxemia could not be explained by an oxygen deficiency. Renal oxygen redistribution could for the first time be demonstrated during fluid resuscitation. HES130/0.4 had no influence on the VO2,ren and restored renal function with the least increase in the amount of renal work.
Highlights
Septic renal failure is often seen in the intensive care unit but its pathogenesis is only partly understood
The loss of kidney function during endotoxemia could not be explained by an oxygen deficiency
Resuscitation with HES200/0.5 (HES-STERIL® 6%) and Ringer's lactate restored the mean arterial pressure (MAP) to baseline values, whereas after resuscitation with HES130/0.4 (Voluven®) the MAP remained at 96 ± 26 mmHg
Summary
Septic renal failure is often seen in the intensive care unit but its pathogenesis is only partly understood. Sepsis seems to have an additional impact on outcome, as mortality can be up to 75% among patients with acute septic renal failure [2,3]. The pathogenesis of sepsis-induced renal failure is multifactorial and is characterized by a reduction in the glomerular filtration rate that may occur despite a maintained renal blood flow (RBF) and normal systemic hemodynamics [4]. Theories on the pathogenesis suggest an uncontrolled and inappropriate release of various inflammatory mediators leading to direct cytotoxic effects or an impairment of the microvascular autoregulation [6]. The latter might cause a maldistribution of renal microcirculatory blood flow and oxygen supply.
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