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大鼠非复苏性失血性休克期间白蛋白结合伊文思蓝的器官特异性外渗

Organ-specific extravasation of albumin-bound Evans blue during nonresuscitated hemorrhagic shock in rats.

作者信息

Schumacher Jan, Binkowski Kathrin, Dendorfer Andreas, Klotz Karl-Friedrich

机构信息

Department of Anesthesiology, University of Luebeck, Luebeck, Germany.

出版信息

Shock. 2003 Dec;20(6):565-8. doi: 10.1097/01.shk.0000093540.78705.71.

DOI:10.1097/01.shk.0000093540.78705.71
PMID:14625482
Abstract

Shock-induced enhanced capillary permeability is associated with alterations in the interstitial matrix composition and contributes to organ damage. This study was designed to evaluate albumin extravasation in various organ tissues during severe, hemorrhagic shock without fluid resuscitation and reperfusion. Target value of hemorrhagic shock was a reduction of cardiac output (CO) by 50% induced by removal of blood. Twelve anesthetized Sprague-Dawley rats (260-325 g) kept under continuous hemodynamic monitoring were randomly assigned to a group of hemorrhagic shock (n = 6) and a control group of normovolemic animals (n = 6). After 30 min of shock 50 mg/kg b.w. Evans blue (EB) was injected intravenously followed by an incubation period of 20 min. Exsanguination and wash out of the intravascular space was performed by a pressure-controlled perfusion with heparinized saline before harvesting organs to quantify albumin-bound EB extravasation. We found that withdrawal of 4.7 +/- 0.4 mL (mean, +/-SEM) blood, which accounts for 21.1% of the calculated total blood volume, resulted in a reduction of CO from 36.1 +/- 3.1 to 19.4 +/- 2.7 mL/min. Simultaneously, MAP decreased from 98 +/- 6 to 40 +/- 1 mmHg. In hemorrhaged rats, the interstitial concentration of EB in lung and kidney was significantly higher than observed in intact animals, whereas heart, spleen, liver, ileum, skeletal muscle, and skin showed no significant microvascular damage. We conclude that despite the absence of fluid resuscitation and reperfusion, microvascular damage in lung and kidney is evident within the first thirty minutes of hemorrhagic shock.

摘要

休克诱导的毛细血管通透性增强与细胞外基质成分改变有关,并导致器官损伤。本研究旨在评估在严重失血性休克且未进行液体复苏和再灌注的情况下,各种器官组织中的白蛋白外渗情况。失血性休克的目标值是通过放血使心输出量(CO)降低50%。将12只持续接受血流动力学监测的麻醉Sprague-Dawley大鼠(260-325克)随机分为失血性休克组(n = 6)和血容量正常动物对照组(n = 6)。休克30分钟后,静脉注射50毫克/千克体重的伊文思蓝(EB),随后孵育20分钟。在收获器官之前,通过用肝素化盐水进行压力控制灌注来放血并冲洗血管内空间,以量化与白蛋白结合的EB外渗情况。我们发现,抽取4.7±0.4毫升(平均值,±标准误)血液,占计算出的总血容量的21.1%,导致CO从36.1±3.1降至19.4±2.7毫升/分钟。同时,平均动脉压(MAP)从98±6降至40±1毫米汞柱。在失血大鼠中,肺和肾中EB的间质浓度显著高于未受损动物,而心脏、脾脏、肝脏、回肠、骨骼肌和皮肤未显示明显的微血管损伤。我们得出结论,尽管未进行液体复苏和再灌注,但在失血性休克的前30分钟内,肺和肾的微血管损伤明显。

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