摘要
目的探讨异丙酚对失血性休克再灌注后胃黏膜损伤的作用及其机制。方法成年新西兰雄性大白兔75只,随机分为对照组、模型组及缺血前(P1)、再灌注前(P2)和再灌注后(P3)应用异丙酚组,每组15只。建立失血性休克再灌注胃黏膜损伤(HR-GMI)模型。P1、P2及P3组分别于缺血前、再灌注前10min及再灌注后20min静脉注射异丙酚5mg/kg后,以20mg·kg^-1·h^-1持续泵人,对照组和模型组给予等量生理盐水。观察胃黏膜细胞超微结构的改变,并检测胃黏膜和血清中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量的变化。结果①模型组胃黏膜主细胞线粒体大部分嵴和膜融合或消失,呈空泡化或空泡样变,粗面内质网有脱颗粒现象,而各异丙酚组线粒体及粗面内质网变化减轻,尤以P1组变化最小。②与对照组比较,模型组胃黏膜和血清中SOD活性明显降低,而MDA含量显著升高(P均〈0.01);与模型组比较,各异丙酚组胃黏膜和血清中SOD活性升高,而MDA含量降低(P〈0.05或P〈0.01);与P3组比较,P1组SOD活性升高,MDA含量降低(P均〈0.05)。结论异丙酚可减轻失血性休克再灌注兔胃黏膜损伤,其机制可能与清除氧自由基及抑制氧自由基产生有关。
Objective To study the therapeutic effect and its mechanisms of propofol on gastric mucosal injury after hemorrhagic shock with reperfusion in rabbits. Methods Seventy-five New Zealand healthy adult male rabbits were randomly divided into 5 groups of 15 rabbits each: control group (S group), model group (M group), pre-ischemia group (P1 group ), pre-reperfusion group (P2 group ) and post-reperfusion group (P3 group). The hemorrhage reperfusion-gastric mucosal injury (HR-GMI) model was reproduced. In P1, P2 and P3 groups, propofol 5 mg/kg was injected intravenously 10 minutes before ischemia, reperfusion and 20 minutes after reperfusion respectively, then propofol 20mg·kg^-1·h^-1 was infused. In control and model groups, propofol Was replaced with equal volume of normal saline. The uhramicrostructural change in gastric mucosa was examined, and the activity of superoxide diamutase (SOD) and contents of malondialdehyde (MDA) in serum and gastric mucosa were determined. Results①In M group, the most of the cristae and membranes of mitochondria in chief cells of gastric mucosa were fused or disappeared, with formation of vacuoles which induced vacuolization, and a part of membrane blended or disappeared, and degranulation appeared in rough endoplasmic reticulum in these cells. These changes in mitochondria and rotigh endoplasmic reticulum were mitigated in all propofol groups ,especially in P1 group.②The activity of SOD was significantly decreased and the contents of MDA were obviously increased in serum and gastric mucosa in M group compared with those in S group (all P〈0. 01). The activity of SOD was significantly increased and the content of MDA was decreased in serum and gastric mucosa in all propofol groups compared with those in M group (P〈0. 05 or P〈0. 01). The activity of SOD was higher and the content of MDA was lower in P1 group than those in P3 group (both P〈0. 05). Conclusion Propofol can attenuate the gastric mucosa injury by eliminating oxygen free radical and preventing its generation caused by hemorrhagic shock and reperfusion.
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2008年第3期180-182,F0003,共4页
Chinese Critical Care Medicine
基金
基金项目:河北省科研究与发展计划资助项目(05276101D-41)
关键词
异丙酚
失血性休克
再灌注损伤
胃黏膜
氧自由基
propofol
hemorrhagic shock
reperfusion injury
gastric mucosa
oxygen free radical