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作 者:吴远波[1] 李建国[1] 王丽[1] 周青[1] 贾宝辉[1]
机构地区:[1]武汉大学中南医院ICU,湖北武汉430071
出 处:《武汉大学学报(医学版)》2008年第1期5-8,共4页Medical Journal of Wuhan University
基 金:国家自然科学基金资助项目(编号:30672727)
摘 要:目的:观察烟碱对内脏动脉阻断性(SAO)休克大鼠总体生存率、颈动脉平均动脉压(MAP)、血气分析及乳酸值的影响,探讨胆碱能抗炎通路在SAO休克中的作用。方法:采用阻断肠系膜上动脉和腹腔干动脉复制SAO休克模型。30只健康雄性大鼠随机分为5组:对照组(假手术组)、SAO组、烟碱组、六烃季胺组和α银环蛇毒素(α-BGT)组,每组6只。实验期间连续观察平均动脉压,再灌注1 h后取血行血气分析和乳酸值检测。另取30只SD大鼠随机分为对照组、SAO组和烟碱组,每组10只,记录3组大鼠4 h总体生存率和平均生存时间。结果:与假手术组比较,SAO组平均生存时间显著缩短,各时间点的生存率均显著降低(均为P<0.01);再灌注后MAP持续低下,并有严重的代谢性酸中毒和高乳酸血症。与SAO组比较,烟碱组平均生存时间延长,各时间点的生存率均显著提高(均为P<0.01);再灌注后MAP下降幅度减轻,代谢性酸中毒缓解。经六烃季胺及-αBGT拮抗后,烟碱处理的上述效应则完全抵消。结论:烟碱能够提高整体生存率,逆转SAO休克中严重低血压,改善休克状况,减轻酸中毒。其作用机制可能与激活胆碱能抗炎通路有关。Objective: To investigate the protective effect of nicotine in rats subjected to splanehnie artery occlusion (SAO) shock. Methods: Thirty male Sprague-Dawley rats were randomly divided into five groups (n=6 in each group) as sham group, SAO group, nicotine group, nicotinic antagonist (NAA) group and α-BGT group. SAO shock was induced by clamping both the superior mesenteric artery (SMA) and the celiac trunk for 45 min, followed by reperfusion for 60 min. Nicotine dissolved in normal saline was administered via vena caudalis 15 min after artery occlusion. All the animals were implanted with catheter into left common carotid artery to connect pressure transducer for continuous monitoring MAP. Blood gas analysis and lactic acid were assayed at 1 h after reperfusion. Another 30 rats were randomly divided into sham group, SAO group and nicotine group for observing survival time and survival rate. Results: Nicotine could significantly revert the marked hypotension in the period of reperfusion, reduce the survival time and raise the survival rate, greatly decrease the blood lactic acid concentration, improve the metabolic acidosis on rat subject SAO shock, but no such effects were found in NAA group and α-BGT group. Conclusion: The results suggest that nicotine might produce a protective effect on SAO shock rats. The mechanism maybe relate to the activation of cholinergic anti-inflammatory pathway.
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