Département d'Anesthésie Réanimation, Equipe Accueil Inserm 4564 Université Paul Sabatier Toulouse III, CHU Purpan, Toulouse, France.
Crit Care Med. 2011 Sep;39(9):2131-8. doi: 10.1097/CCM.0b013e31821f04f0.
Sparse data are available on renal consequences of hemorrhagic shock in mice. This study aimed to extend the current knowledge on functional and morphologic renal impact of hemorrhagic shock in mice and to determine its ability to stand as an accurate model of acute kidney injury.
In vivo study.
University research unit.
C57/Bl6 mice.
A model of controlled hemorrhagic shock was adapted to determine the renal impact of hemorrhagic shock in mice.
Renal functions and kidney morphology were followed up from 3 hrs to 21 days after hemorrhagic shock. When prolonged up to 2 hrs, hypotension (35 mm Hg mean arterial blood pressure) induced by temporary blood removal was responsible for an early and lasting increase in hypoxia-inducible factor-1α and kidney-inducible molecule-1 gene expression that paralleled acute tubular necrosis and renal failure. Two-hr hypotension induced an important but reversible decrease in glomerular filtration rate up to 6 days after hemorrhagic shock. Other renal dysfunctions included a renal loss of sodium, assessed by the increase in sodium excretion, and a decrease in urine concentration that persists up to day 21. Tissular damages prevailed in the outer medulla 2 days after hemorrhagic shock, being maximal at day 6. At day 21, renal healing was associated with epithelial recovery and a significant interstitial fibrosis.
Our data indicate that apparent recovery of renal function after acute kidney injury can mask persisting dysfunctions and tissular damages that could predispose to chronic kidney disease. Prolonged hemorrhagic shock in mice closely mimics renal effects induced by similar situation in humans, thus providing a useful tool to investigate pathophysiological mechanisms and protection strategies against acute kidney injury in situations such as hemorrhagic shock.
关于出血性休克对小鼠肾脏影响的相关数据较为缺乏。本研究旨在深入了解出血性休克对小鼠肾脏功能和形态的影响，并确定其作为急性肾损伤模型的准确性。
体内研究。
大学研究单位。
C57/Bl6 小鼠。
采用控制性出血性休克模型来确定出血性休克对小鼠肾脏的影响。
从出血性休克后 3 小时到 21 天，监测肾脏功能和肾脏形态。当低血压（平均动脉压 35mmHg）持续 2 小时时，临时失血导致的低血压会导致早期和持续的缺氧诱导因子-1α和肾脏诱导分子-1基因表达增加，这与急性肾小管坏死和肾衰竭相平行。2 小时的低血压会导致肾小球滤过率在出血性休克后 6 天内出现重要但可恢复的下降。其他肾脏功能障碍包括通过钠排泄增加评估的肾失钠，以及尿液浓缩功能下降，可持续至第 21 天。出血性休克后 2 天，外髓质组织损伤明显，第 6 天达到高峰。第 21 天，肾脏愈合与上皮细胞恢复和间质纤维化显著相关。
我们的数据表明，急性肾损伤后肾功能的明显恢复可能掩盖持续存在的功能障碍和组织损伤，从而增加慢性肾脏病的风险。小鼠长时间的出血性休克可模拟人类类似情况下的肾脏效应，因此为研究出血性休克等情况下的急性肾损伤的病理生理机制和保护策略提供了有用的工具。
