Influence of fluid resuscitation on renal microvascular PO(2 )in a normotensive rat model of endotoxemia

INTRODUCTION: Septic 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 PO(2 )(μPO(2)) and oxygen consumption (VO(2,ren)), that endotoxemia is associated with a diminished kidney function, that fluid resuscitation can restore μPO(2), VO(2,ren )and kidney function, and that colloids are more effective than crystalloids. METHODS: Male 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 μPO(2 )in the cortex and medulla and the renal venous PO(2 )were measured by a recently published phosphorescence lifetime technique. RESULTS: Endotoxemia induced a reduction in renal blood flow and anuria, while the renal μPO(2 )and VO(2,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 VO(2,ren), in contrast to HES130/0.4. CONCLUSION: The 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 VO(2,ren )and restored renal function with the least increase in the amount of renal work.