L-NAME对感染性休克大鼠心功能变化和血管张力变化的影响  

Effect of L-NAME on Hemodynamic Parameters and Thoracic Aorta Tension in Rats with Septic Shock

作　　者：夏满莉[1,2] 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,浙江杭州310031

出　　处：《嘉兴学院学报》2009年第3期51-56,共6页Journal of Jiaxing University

基　　金：嘉兴市科技局资助项目(2005AY3044)

摘　　要：探讨一氧化氮合酶(nitric oxide synthase,NOS)抑制剂左旋硝基精氨酸甲酯(N-ωnitro-L-ar-ginine methyl ester hydrochloride,L-NAME)对感染性休克大鼠心功能变化和血管张力变化的影响.采用盲肠结扎和穿孔法(cecal ligation and puncture,CLP)建立大鼠感染性休克模型;在体颈动脉插管和心室内导管术,测定血压和心室动力学指标;用离体血管灌流方法,测定大鼠胸主动脉环的张力.CLP诱发的感染性休克各个时期大鼠血压与左心室动力学指标与对照组有显著差异;CLP晚期组胸主动脉环对苯肾上腺素(phenylephrine,PE)和KCl诱导的收缩反应量效曲线明显低于假手术组(Sham),由PE及随后加入的CaCl2所引起的收缩幅度则明显低于Sham组,最大反应降低;L-NAME给药干预能降低CLP感染性休克大鼠的死亡率,显著改善其血压和左心室动力学各项指标,并使其胸主动脉环的收缩能力恢复或超过Sham组的水平.NO的过量产生可能是导致感染性休克心功能变化和血管低反应性的主要原因,一氧化氮合酶非特异性阻断剂(L-NAME)给药干预,可明显抑制感染性休克心功能恶化和血管收缩反应性的下降.AIM： To determine the effect of L NAME on hemodynamic parameters and thoracic aorta tension in rats with septic shock. METHODS： we used cecal ligation and puncture （CLP） method to establish the model of shocked rats, and L NAME, the nitric oxide synthase inhibitor, was injected after CLP. The carotid artery was cannulated and connected to a pressure transducer to determine mean arterial blood pressure（ MABP）. Ventricular dynamic parameters were determined following intraventrieular cannulation via the carotid artery. Isolated thoracic rings were mounted on the organ bath and the tension of the vessel was recorded. RESULTS： L NAME significantly improved MABP and ventricular dynamic parameters in septic shocked rats. Vasoconstriction to PE, KCL, and Ca^2＋ was also markedly increased by L NAME in the rats. CONCLUSIONS： The results indicate that overproduction of nitric oxide may mediate the change of hemodynamic parameters and the vascular hyporeactivity in the shocked rats induced by CLP, and L NAME inhibited the decrease of hemodynamic parameters and vasoconstriction in CLP these rats.

关 键 词：L—NAME 感染性 休克 大鼠 血流动力学 主动脉 一氧化氮 

分 类 号：R540.4[医药卫生—心血管疾病]