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目的 :探讨川芎嗪对失血性休克再灌注后肠粘膜屏障功能的保护作用。方法 :30只日本大耳白兔随机分为 3组 :假手术组 (A组 ) ,单纯休克组 (B组 ) ,川芎嗪治疗组 (C组 )。以硫代巴比妥酸比色法、放射免疫法及硝酸还原酶法测定末端回肠粘膜丙二醛 (MDA)、肿瘤坏死因子 (TNFα)、白细胞介素 - 1β(IL - 1β)及一氧化氮代谢产物(NO-2 /NO-3 )含量 ,并取体循环血做细菌培养 ,取肠粘膜行光镜和电镜观察。结果 :B组肠粘膜MDA、TNFα、IL - 1β含量明显高于A组 ,NO-2 /NO-3 浓度显著低于A组 ,而C组变化无显著 ;B组细菌移位率明显高于A组 ,而C组与A组比较无显著差异 ;B组肠粘膜损伤明显重于A组 ,C组明显轻于B组 ,而C组与A组差异无显著。结论 :川芎嗪能保护失血性休克再灌注后肠粘膜屏障功能 ,这可能与其清除体内氧自由基、提高一氧化氮水平及阻抑炎性介质作用有关
Objective: To explore the protective effect of tetramethylpyrazine on intestinal mucosal barrier function after hemorrhagic shock and reperfusion. Methods: Thirty Japanese white rabbits were randomly divided into three groups: sham operation group (group A), simple shock group (group B), and tetramethylpyrazine treatment group (group C). Determination of Malondialdehyde (MDA), Tumor Necrosis Factor (TNFα), Interleukin-1β (IL-1β) and Nitric Oxide in the Terminal Ileum Mucosa by Thiobarbituric Acid Colorimetric Method, Radioimmunoassay, and Nitrate Reductase Method The content of nitrogen metabolites (NO-2/NO-3) was taken and the body circulation blood was taken for bacterial culture. The intestinal mucosa was removed and observed under a light microscope and an electron microscope. Results: The contents of MDA, TNFα and IL-1β in intestinal mucosa of group B were significantly higher than those in group A. The concentration of NO-2/NO-3 was significantly lower than that of group A, but there was no significant change in group C. The bacterial translocation rate in group B was significantly higher than that in group B. In group A, there was no significant difference between group C and group A. Intestinal mucosal injury in group B was significantly heavier than that in group A, and group C was significantly lighter than group B. There was no significant difference between group C and group A. Conclusion: Tetramethylpyrazine can protect intestinal mucosal barrier function after hemorrhagic shock and reperfusion, which may be related to its role in removing oxygen free radicals, increasing nitric oxide levels, and suppressing inflammatory mediators.