Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemia.
Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemia.
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DOI：
10.1186/cc4948
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Ince C
中科院分区：
文献类型：
--
作者：
Johannes T;Mik EG;Nohé B;Raat NJ;Unertl KE;Ince C
脓毒性肾衰竭常见于重症监护室，但其发病机制仅部分了解。本研究在一个血压正常的内毒素血症大鼠模型中进行，验证了内毒素血症损害肾脏微血管PO2 （μPO2）和耗氧量（VO2,ren）的假设，内毒素血症与肾功能减退有关，液体复苏可以恢复μPO2， VO2，ren和肾功能，胶体比晶体更有效。雄性Wistar大鼠静脉输注脂多糖1小时，随后用HES130/0.4 （Voluven®）、HES200/0.5 （HES-STERIL®®6%）或乳酸林格氏液进行复苏。用新近发表的磷光寿命法测定肾皮质、髓质和肾静脉的μPO2。内毒素血症引起肾血流量减少和无尿，而肾μPO2和VO2，ren保持相对不变。复苏使肾血流量、肾氧输送和肾功能恢复到基线值，并且与使用不同化合物的氧再分配显示不同模式有关。与HES130/0.4相比，HES200/0.5和林格乳酸增加了VO2。内毒素血症期间肾功能的丧失不能用缺氧来解释。肾氧再分配首次在液体复苏中得到证实。HES130/0.4对VO2、ren和肾功能恢复无影响，对肾功的增加最小。
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 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. 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 μPO2 in the cortex and medulla and the renal venous PO2 were measured by a recently published phosphorescence lifetime technique. Endotoxemia 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. 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 VO2,ren and restored renal function with the least increase in the amount of renal work.
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