Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemiaReportar como inadecuado




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Critical Care

, 10:R88

First Online: 19 June 2006Received: 28 February 2006Accepted: 12 May 2006

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.

AbbreviationsClearcrea= creatinine clearance

cμPO2= cortical microvascular PO2

LPS= lipopolysaccharide

MAP= mean arterial pressure

mμPO2= medullary microvascular PO2

μPO2= microvascular PO2

O2ERren= renal oxygen extraction

PO2= partial pressure of oxygen

PrvO2= renal venous PO2

RBF= renal blood flow

TNa+= tubular sodium reabsorption

VO2,ren= renal oxygen consumption

Electronic supplementary materialThe online version of this article doi:10.1186-cc4948 contains supplementary material, which is available to authorized users.

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Autor: Tanja Johannes - Egbert G Mik - Boris Nohé - Nicolaas JH Raat - Klaus E Unertl - Can Ince

Fuente: https://link.springer.com/







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