Cryer Henry M, Gosche John, Harbrecht Jeff, Anigian Greg, Garrison Neal
Department of Surgery, University of California Los Angeles Medical Center, 10833 Le Conte Ave., 72-178 CHS, Los Angeles, CA 90095, USA.
Am J Surg. 2005 Aug;190(2):305-13. doi: 10.1016/j.amjsurg.2005.05.032.
Decompensated hemorrhagic shock is often refractory to resuscitation, and we show here that it is associated with loss of vascular tone in skeletal muscle precapillary arterioles. We tested the hypothesis that microvascular derangements in the skeletal muscle, intestinal, and renal microcirculation systems would be reversed by initial hypertonic saline-dextran infusion.
Male Sprague-Dawley rats underwent precollicular brain stem transection without anesthesia for study. Parameters measured by in vivo videomicroscopy included cardiac output, mean arterial pressure, and microvascular responses in the skeletal muscle, ileum, and renal (i.e., the hydronephrotic kidney) microcirculation systems. Hemorrhaged was induced to a mean arterial pressure of 50 mmHg until decompensation occurred. The rats were then initially resuscitated with (1) 4 mL/kg 7.5% NaCl in 6% dextran 70, (2) 33 mL/kg .9% NaCl in 6% dextran 70, or (3) 33 mL/kg .9% NaCl. Twenty minutes later they received shed blood plus 33 mL/kg .9% NaCl to maintain mean arterial pressure at baseline levels.
Decompensated hemorrhagic shock decreased cardiac output to between 24% and 35% of baseline values and profoundly decreased microvascular blood flow to between 10% and 19% of baseline. At the completion of resuscitation cardiac output increased to greater than baseline in all groups. Microvascular blood flow increased toward baseline transiently but then progressively deteriorated to between 36% and 69% of baseline in the 3 tissues. There was no significant difference between the three resuscitative fluids.
Despite return of cardiac output to greater than baseline levels, muscle, intestinal, and renal microvascular blood flows remained significantly depressed. Hypertonic saline and/or dextran did not improve these deficits.
失代偿性失血性休克常常对复苏治疗具有抵抗性，我们在此表明，它与骨骼肌毛细血管前微动脉血管张力丧失有关。我们检验了这样一个假设，即通过初始输注高渗盐水-右旋糖酐可逆转骨骼肌、肠道和肾脏微循环系统中的微血管紊乱。
雄性Sprague-Dawley大鼠在未麻醉状态下接受颈前脑干横断术以进行研究。通过体内视频显微镜测量的参数包括心输出量、平均动脉压以及骨骼肌、回肠和肾脏（即肾积水肾脏）微循环系统中的微血管反应。诱导出血使平均动脉压降至50 mmHg，直至出现失代偿。然后大鼠首先用以下溶液进行复苏：(1) 4 mL/kg 7.5%氯化钠加6%右旋糖酐70；(2) 33 mL/kg 0.9%氯化钠加6%右旋糖酐70；或(3) 33 mL/kg 0.9%氯化钠。20分钟后，它们接受回输的血液加33 mL/kg 0.9%氯化钠，以将平均动脉压维持在基线水平。
失代偿性失血性休克使心输出量降至基线值的24%至35%之间，并使微血管血流量大幅降至基线的10%至19%之间。复苏结束时，所有组的心输出量均增加至高于基线水平。微血管血流量短暂地向基线增加，但随后在这3个组织中逐渐恶化至基线的36%至69%之间。三种复苏液体之间无显著差异。
尽管心输出量恢复至高于基线水平，但肌肉、肠道和肾脏的微血管血流量仍显著降低。高渗盐水和/或右旋糖酐并未改善这些缺陷。
