...
首页> 外文期刊>Acta Anaesthesiologica Scandinavica >Effects of surfactant replacement on alveolar overdistension and plasma cytokines in ventilator-induced lung injury
【24h】

Effects of surfactant replacement on alveolar overdistension and plasma cytokines in ventilator-induced lung injury

机译:表面活性剂替代对呼吸机诱发肺损伤中肺泡过度扩张和血浆细胞因子的影响

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Background: Overdistension of the lung causes ventilator-induced lung injury (VILI) accompanied by surfactant abnormalities and inflammatory changes. We investigated the effects of surfactant replacement on overdistension of the terminal airspaces and plasma cytokine levels in VILI. Methods: VILI was induced by high-pressure ventilation (HPV) in rats anesthetized with pentobarbital, followed by ventilation for 2 h in the maintenance mode (tidal volume = 10 ml/kg, positive end-expiratory pressure = 7.5cmH_2O) with or without surfactant replacement. The sizes of the terminal airspaces were determined after fixing the lungs at an airway pressure of 10cmH_2O on deflation. Cytokine levels were assessed by enzyme-linked immunosorbent assay. Results: The mean ratio of the largest terminal airspace size class (>= 64,000 mum~2) was increased from 13.4% to 32.0% by HPV (P<0.05). After maintenance-mode ventilation, the ratio decreased to 16.1% with surfactant replaceent (P<0.05), but increased to 44.6% without surfactant replacement (P<0.05). Mean macrophage inflammatory protein-2 (MIP-2) levels in the plasma increased from <0.02 to 6.9ng/ml with HPV (P<0.05), and further increased to >= 11.8ng/ml, regardless of surfactant replacement after maintenance-mode ventilation. Similar tendencies were observed in the interleukin (IL)-6 and IL-10 levels. Tumor necrosis factor-alpha levels were almost negligible during the experiment. Conclusion: In rats with VILI, surfactant replacement reversed overdistension of the terminal airspaces that may induce barotrauma, but not upregulation of MIP-2, IL-6, and IL-10 within 2 h.
机译:背景:肺部过度扩张会导致呼吸机诱发的肺损伤(VILI),并伴有表面活性剂异常和炎症变化。我们调查了表面活性剂替代对终端空域过度扩张和VILI中血浆细胞因子水平的影响。方法:高压通气(HPV)诱导戊巴比妥麻醉大鼠VILI,然后在维持模式(潮气量= 10 ml / kg,呼气末正压= 7.5cmH_2O)下通气2 h表面活性剂替代。在放气时将肺部固定在气道压力为10cmH_2O的情况下,确定最终空域的大小。通过酶联免疫吸附测定法评估细胞因子水平。结果:HPV使最大终端空域尺寸类别(> = 64,000 mum-2)的平均比率从13.4%增加到32.0%(P <0.05)。维持模式通风后,使用表面活性剂替代剂时该比例降低至16.1%(P <0.05),但不使用表面活性剂替代剂时该比例增加至44.6%(P <0.05)。血浆中巨噬细胞炎性蛋白2(MIP-2)的平均水平从HPV从<0.02增至6.9ng / ml(P <0.05),并进一步增至> = 11.8ng / ml,无论维持后是否更换表面活性剂-模式通风。在白介素(IL)-6和IL-10水平也观察到类似趋势。在实验过程中,肿瘤坏死因子的水平几乎可以忽略不计。结论:在患有VILI的大鼠中,表面活性剂替代可逆转终末气隙的过度扩张,这可能会引起气压伤,但在2 h内不会上调MIP-2,IL-6和IL-10。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号