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作 者:纪存良[1] 林长赋[1] 李文志[1] 岳子勇[1] 路莉[1]
机构地区:[1]哈尔滨医科大学附属第二医院麻醉科
出 处:《临床麻醉学杂志》2004年第7期413-415,共3页Journal of Clinical Anesthesiology
摘 要:目的 探讨丙泊酚对大鼠肠缺血 再灌注损伤的作用及其机制。方法 30只Wistar大鼠随机分为肠缺血 再灌注组 (IIR组 )、丙泊酚组 (P组 )和假手术组 (S组 ) ,每组 10只。记录各组平均动脉压 (MAP)、动态肺顺应性 (Cdyn) ,测量再灌注 12 0min时门静脉血内毒素 (ET)、腔静脉血肿瘤坏死因子α(TNF α)、白细胞介素 8(IL 8)以及肺灌洗液 (BALF)中总蛋白 (TP)和磷脂 (Lip)的含量。结果 S组的检测指标在整个实验中未见明显变化。再灌注后P组和IIR组的MAP、Cdyn呈进行性下降 (与S组比 ,P <0 0 5 ) ,再灌注 12 0min时两组的门静脉血ET ,腔静脉血TNF α、IL 8浓度升高显著 (与S组比 ,P <0 0 5 ) ,尤以IIR组显著 (与P组比 ,P <0 0 5 )。P组BALF中TP、Lip含量与S组比较无显著差异 (P >0 0 5 ) ;IIR组与S组比较TP含量升高 ,Lip含量减少 (P <0 0 5 )。结论 丙泊酚能减轻大鼠肠缺血 再灌注损伤后的内毒素移位和细胞因子反应并对肺损伤有保护作用 ,可能与其抗氧化潜能。Objective To investigate the effects of propofol on intestinal ischemia-reperfusion injury and its mechanism.Methods Thirty Wistar rats weighing 325-375 g were randomly divided into three groups : sham operation group(S),intestinal ischemia reperfusion group (IIR)and propofol group(P). Intestinal ischemia was produced by clamping the superior mesenteric artery (SMA) for 45 min and reperfusion was allowed for 120 min after SMA unclamped.MAP and dynamic compliance of the lungs(Cdyn)were recorded. Blood samples were taken from portal vein and right external jugular vein at 120 min after I/R for the measurements of endotoxin (ET), tumor necrosis factor alpha (TNF-α)and interleukin 8 (IL-8)concentration.Animals were sacrificed at 120 min after I/R and analyzed by bronchoalveolar lavage for the contents of total protein (TP) and phospholipid (Lip) in bronchoalveolar lavage fluid (BALF). Results There were no significant changes in all parametric values in group S during the whole experiment. But MAP and Cdyn in the other two groups decreased after I/R.Cdyn decreased significantly in group IIR [from (0.48±0.02) ml/cmH 2O to(0.28±0.02) ml/cmH 2O] than that in group P [from (0.49±0.02) ml/cmH 2O to (0.35±0.01) ml/cmH 2O], ET increased more markedly in group IIR[ (1.17±0.18) EU/ml] than that in group P[ (0.74±0.13) EU/ml]and that in group S[(0.25±0.12) EU/ml]. In both groups undergone intestinal I/R, TNF-α and IL-8 increased and propofol administration before I/R attenuated the increase of IL-8 but not TNF-α. TP was increased higher by I/R in group IIR than that in group P,and propofol administration blunted the intestinal I/R induced decrease in Lip. There were no significant differences in TP and Lip between group S and group P. Conclusions Propofol has protective effects on the endotoxin translocation and lung injury induced by intestinal I/R, which may be related to the antioxidation and the effects on PMN and cytokines.
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