Hypertonic saline resuscitation improves intestinal micro circulation in a rat model of hemorrhagic shock
Hypertonic saline resuscitation improves intestinal micro circulation in a rat model of hemorrhagic shock
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DOI：
10.1016/j.surg.2006.05.015
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发表时间：
2006-10-01
期刊：
影响因子：
3.8
通讯作者：
Garrison, R. Neal
中科院分区：
文献类型：
--
作者：
Zakaria, El Rasheid;Tsakadze, Nina L.;Garrison, R. Neal
背景资料。失血性休克(HS)的常规复苏(CR)通常能恢复和维持血流动力学，但不能恢复肠道灌流。CR后肠缺血与肠源性全身性炎症反应的启动和HS后进行性器官衰竭有关。我们提出高渗盐水复苏(HTSR)可以预防肠缺血。麻醉雄性SD大鼠(200~215g)失血至平均动脉压(MAP)的50%，持续60min，随机分为复苏I组(n=7)：I组：假手术+HS；II组：HS+CR放血+2体积生理盐水(NS)；III组：HS+放血+高渗盐水(HTS)；(7.5%氯化钠，4ml/kg)；IV组：HS+HTS，60min后恢复放血；IV组：HS+HTS组，60min后给予1体积生理盐水。用在体视频显微镜和光学多普勒测速仪测量回肠末端流入动脉(A1)、近端和远端丝裂前小动脉(A3)的微血管直径以及A1处的血流。II组和III组分别测定红细胞压积、血浆渗透压和电解质。HS引起AI小动脉的选择性血管收缩，而粘膜前小动脉则未见此作用。CR恢复并维持MAP，并引起与低灌注量相关的所有肠小动脉水平的全身性、进行性血管收缩。HTSR未能恢复或维持MAP或肠A1动脉血流量，直到失血回流。然而，HTSR阻止了复苏后、粘膜前的血管收缩，并在A3小动脉产生了一种潜伏的选择性血管扩张，这在早期回血时最为显著(组III)。这种选择性小动脉血管活动与内皮细胞功能的显著改善有关。血浆高渗和高钠血症在HTS复苏后2小时内持续存在。小容量HTSR可用作创伤现场的复苏方案，也可用于需要低血压复苏的选择性临床情况。HTSR通过选择性扩张毛细血管前小动脉来改善肠道灌注量，即使在接近休克水平时也是如此。
Background. Conventional resuscitation (CR) from hemorrhagic shock (HS) often restores and maintains hemodynamics but fails to restore intestinal perfusion. Post-CR intestinal ischemia has been implicated in the initiation of a gut-derived exaggerated systemic inflammatory response and in the progressive organ failure following HS. We propose that intestinal ischemia can be prevented with hypertonic saline resuscitation (HTSR).Methods. Anesthetized male Sprague-Dawley rats (200 to 215 g) were hemorrhaged to 50% of mean arterial pressure (MAP) for 60 minutes and randomly assigned to I of the resuscitation groups (n = 7 each): Group I: sham operation and no HS; Group II: HS + CR with the return of the shed blood + 2 volumes of normal saline (NS); Group III: HS + return of the shed blood + hyperionic saline (HTS); (7.5 % NaCl, 4 ml/kg); Group IV: HS + HTS, then return of the shed blood after 60 minutes; Group IV: HS + HTS, then 1 volume of NS after 60 minutes. Microvascular diameters Of inflow (A1) and proximal and distal premitcosal arterioles (A3) in terminal ileum and flow in A1 were measured using in vivo videomicroscopy and optical Doppler velocimetry. Hematocrit, plasma osmolarity, and electrolytes were measured in Groups II and III.Results. HS caused a selective vasoconstriction in A I arterioles that was not seen in the premucosal arterioles. CR restored and maintained MAP and caused generalized, progressive vasoconstriction at all intestinal arteriolar levels that is associated with hypoperfusion. HTSR failed to restore or maintain MAP or intestinal A1 arteriolar blood flow until the shed blood was returned. However, HTSR prevented the post-resuscitation, premucosal vasoconstriction and produced an insidious selective vasodilation in the A3 arterioles, which was most significant with early blood return (Group III). This selective arteriolar vasoactivity was associated with a significant improvement of endothelial cell function. Plasma hyperosmolality and hypernatremia persisted during the entire 2 hours post-resuscitation with HTS.Conclusions. Small-volume HTSR can be used as a resuscitation regimen at the trauma scene and for selective clinical conditions where hypotensive resuscitation is indicated. HTSR improves intestinal perfusion by selective vasodilation of the precapillary arterioles even at MAP close to shock levels.