• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>BMC Anesthesiology >Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury
【24h】

Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury

机译：胸膜硬膜外麻醉可减少内毒素诱导的内皮损伤

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background The sympathetic nervous system is considered to modulate the endotoxin-induced activation of immune cells. Here we investigate whether thoracic epidural anesthesia with its regional symapathetic blocking effect alters endotoxin-induced leukocyte-endothelium activation and interaction with subsequent endothelial injury. Methods Sprague Dawley rats were anesthetized, cannulated and hemodynamically monitored. E. coli lipopolysaccharide (Serotype 0127:B8, 1.5?mg x kg-1 x h-1) or isotonic saline (controls) was infused for 300?minutes. An epidural catheter was inserted for continuous application of lidocaine or normal saline in endotoxemic animals and saline in controls. After 300?minutes we measured catecholamine and cytokine plasma concentrations, adhesion molecule expression, leukocyte adhesion, and intestinal tissue edema. Results In endotoxemic animals with epidural saline, LPS significantly increased the interleukin-1β plasma concentration (48%), the expression of endothelial adhesion molecules E-selectin (34%) and ICAM-1 (42%), and the number of adherent leukocytes (40%) with an increase in intestinal myeloperoxidase activity (26%) and tissue edema (75%) when compared to healthy controls. In endotoxemic animals with epidural infusion of lidocaine the values were similar to those in control animals, while epinephrine plasma concentration was 32% lower compared to endotoxemic animals with epidural saline. Conclusions Thoracic epidural anesthesia attenuated the endotoxin-induced increase of IL-1β concentration, adhesion molecule expression and leukocyte-adhesion with subsequent endothelial injury. A potential mechanism is the reduction in the plasma concentration of epinephrine.
机译：背景技术交感神经系统被认为可调节内毒素诱导的免疫细胞活化。在这里我们调查胸腔硬膜外麻醉及其区域性交感神经阻滞作用是否改变了内毒素诱导的白细胞-内皮细胞的活化以及与随后的内皮损伤的相互作用。方法对SD大鼠进行麻醉，插管和血流动力学监测。将大肠杆菌脂多糖（血清型0127：B8，1.5？mg x kg -1 x h -1 ）或等渗盐水（对照）注入300分钟。插入硬膜外导管以连续向内毒素血症动物和对照组注入利多卡因或生理盐水。 300分钟后，我们测量儿茶酚胺和细胞因子的血浆浓度，黏附分子表达，白细胞黏附和肠组织水肿。结果在硬膜外盐水的内毒素动物中，LPS显着增加了白细胞介素1β血浆浓度（48％），内皮粘附分子E-选择素的表达（34％）和ICAM-1的表达（42％）以及粘附白细胞的数量（40％）与健康对照组相比，肠道髓过氧化物酶活性（26％）和组织水肿（75％）增加。在硬膜外输注利多卡因的内毒素性动物中，该值与对照动物相似，而肾上腺素血浆浓度比硬膜外输注利多卡因的内毒素性动物低32％。结论胸膜硬膜外麻醉可减轻内毒素诱导的IL-1β浓度，粘附分子表达和白细胞粘附的增加，并随后引起内皮损伤。潜在的机制是降低肾上腺素的血浆浓度。

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