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Continuous thoracic epidural anesthesia improves gut mucosal microcirculation in rats with sepsis.

机译:胸连续硬膜外麻醉改善肠道粘膜微循环与脓毒症大鼠。

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摘要

Microcirculatory dysfunction contributes significantly to tissue hypoxia and multiple organ failure in sepsis. Ischemia of the gut and intestinal hypoxia are especially relevant for the evolution of sepsis because the mucosal barrier function may be impaired, leading to translocation of bacteria and toxins. Because sympathetic blockade enhances intestinal perfusion under physiologic conditions, we hypothesized that thoracic epidural anesthesia (TEA) may attenuate microcirculatory perturbations during sepsis. The present study was designed as a prospective and controlled laboratory experiment to assess the effects of continuous TEA on the mucosal microcirculation in a cecal ligation and perforation model of sepsis in rats. Anesthetized Sprague-Dawley rats underwent laparotomy and cecal ligation and perforation to induce sepsis. Subsequently, either bupivacaine 0.125% (n = 10) or isotonic sodium chloride solution (n = 9) was continuously infused via the thoracic epidural catheter for 24 h. In addition, asham laparotomy was carried out in eight animals. Intravital videomicroscopy was then performed on six to ten villi of ileum mucosa. The capillary density was measured as areas encircled by perfused capillaries, that is, intercapillary areas. The TEA accomplished recruitment of microcirculatory units in the intestinal mucosa by decreasing total intercapillary areas (1,317 +/- 403 vs. 1,001 +/- 236 microm2) and continuously perfused intercapillary areas (1,937 +/- 512 vs. 1,311 +/- 678 microm2, each P < 0.05). Notably, TEA did not impair systemic hemodynamic variables beyond the changes caused by sepsis itself. Therefore, sympathetic blockade may represent a therapeutic option to treat impaired microcirculation in the gut mucosa resulting from sepsis. Additional studies are warranted to assess the microcirculatory effects of sympathetic blockade on other splanchnic organs in systemic inflammation.
机译:Microcirculatory障碍贡献显著的组织缺氧和多个在脓毒症器官衰竭。肠道缺氧特别相关的脓毒症的进化,因为粘膜屏障功能受损,导致易位的细菌和毒素。同情封锁增强肠道灌注在生理条件下,我们假设胸硬膜外麻醉(茶)可能减弱microcirculatory在脓毒症扰动。设计前瞻性和控制实验室实验评估的影响连续的茶在粘膜微循环脓毒症的盲肠的结扎和穿孔模型在老鼠身上。进行了剖腹手术和盲肠的结扎穿孔诱发败血症。bupivacaine 0.125% (n = 10)或等渗氯化钠溶液(n = 9)是不断通过胸注入硬膜外导管为24h。此外,阿萨姆剖腹手术在八个动物。然后进行六到十绒毛的回肠粘膜。区域灌注毛细血管包围,intercapillary地区。招聘microcirculatory单位的肠道粘膜总数减少intercapillary地区(1317 + / - 403和1001 + / -236 microm2)和连续灌注intercapillary地区(1937 + / - 512和1311 + / -678个microm2,每个P < 0.05)。损害全身血流动力学变量超出了变化引起的脓毒症本身。同情封锁可能代表一个治疗选择治疗微循环障碍肠道粘膜造成脓毒症。评估的研究是必要的microcirculatory交感阻滞的影响其他的内脏器官系统炎症。

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