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作 者:夏满莉[1] 王敏[1] 柴荣奎[1] 徐策[2] 王会平[2] 夏强[2]
机构地区:[1]嘉兴学院医学院,浙江嘉兴314001 [2]浙江大学医学院生理学系,浙江杭州310058
出 处:《浙江大学学报(医学版)》2010年第6期572-576,共5页Journal of Zhejiang University(Medical Sciences)
基 金:浙江省嘉兴市科技局科研项目资助(2010AY1061)
摘 要:目的:探讨两种败血症模型对大鼠心室动力学及血管张力变化影响的异同。方法:采用盲肠结扎穿孔(CLP)手术20 h致腹膜炎诱导和腹腔注射脂多糖(LPS)6 h诱导败血症模型;在体颈动脉插管和心室内导管术,测定颈动脉血压和左心室动力学指标;用离体血管灌流方法,测定大鼠胸主动脉环的张力。结果:①CLP组大鼠的死亡率为65.2%,LPS组大鼠均存活;②CLP组和LPS组大鼠的血压均显著降低,且CLP组降幅更大(P<0.01);③CLP组和LPS组大鼠的左心室动力学指标心率(HR)、左室发展压(LVDP)和左心室内压最大上升/下降速率(±dP/dtmax)均明显下降(P<0.01),在HR与LVDP两项指标上,CLP组降低程度比LPS组更为明显(P<0.01);④两种模型的内皮完整和去内皮主动脉环对KC l和苯肾上腺素(PE)的收缩反应性均下降(P<0.01),且LPS败血症下降更显著(P<0.01)。结论:两种败血症模型对大鼠心室动力学及血管张力均产生不良后果;CLP败血症在心室动力学方面恶化更加显著;LPS败血症在血管张力方面恶化更加显著。Objective: To compare the ventricular-dynamic parameters and thoracic aorta tension induced by two septic shock models in rats.Methods: Septic shock models were induced by cecal ligation or puncture(CLP) and intraperitoneal injection of lipopolysaccharide(LPS) in rats.The carotid artery was cannulated and connected to a pressure transducer to determine mean arterial blood pressure(MABP).Ventricular dynamic parameters,including heart rate(HR),left ventricular developed pressure(LVDP) and maximal rise/fall velocity of ventricular pressure(±dP/dtmax) were determined.Isolated thoracic rings were mounted on an organ bath and the tension of the vessel was recorded.Results: The mortality was 65.2% in CLP shock rats,but no death in LPS shock rats.The MABP and HR of CLP rats were decreased more prominently than those of LPS rats(P<0.01).Contraction induced by high K+(60 mmol/L) or 10-6 mol/L phenylephrine(PE) in endothelium-intact and endothelium-denuded aortic rings was all attenuated,but in LPS rats it was more prominent(P<0.01).Conclusion: Two rat septic shock models can decrease ventricular-dynamic parameters and vasoconstriction responsiveness of aorta.The ventricular-dynamic parameters decrease more prominently in CLP model,while vasoconstriction responsiveness of aorta changes more in LPS model.
关 键 词:休克 脓毒性 疾病模型 动物 结扎术 盲肠 心室功能 左 败血症 盲肠结扎穿孔 脂多糖类 主动脉 胸 心室动力学
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