败血症休克晚期血管平滑肌细胞钙稳态变化及机制  

The disturbance of calcium metabolism of vascular smooth muscle in the late phase of septic shock and the underlying mechanism

作　　者：丁悦敏[1] 单绮娴[1] 张雄[1] 金红峰[1] 屠洁[1] 夏强[1] 

机构地区：[1]浙江大学医学院生理学教研室,浙江杭州310031

出　　处：《中国病理生理杂志》2003年第11期1484-1487,共4页Chinese Journal of Pathophysiology

基　　金：浙江省留学回国人员基金资助项目 (No.4 1910 0 -N4 0 2 77)

摘　　要：目的 :探讨败血症休克晚期血管平滑肌 (VSM)细胞内钙稳态的变化与血管低反应性的关系及其机制。方法 :采用盲肠结扎和穿孔法 (CLP)复制大鼠败血症休克模型 ,用离体血管灌流方法 ,测定大鼠去内皮主动脉环的张力。结果 :CLP组动脉环对苯肾上腺素 (PE)和KCl的收缩反应均低于假手术组 (Sham) ;CLP组动脉环的钙浓度-收缩曲线比Sham组明显右移 ;在无钙液中 ,CLP组动脉环对咖啡因诱导的收缩幅度与Sham组比无显著差异 ,而由PE及随后加入的CaCl2 所引起的收缩幅度则明显低于Sham组 (P <0 .0 5 )。预先用特异性的一氧化氮合酶抑制剂氨基胍孵育后 ,CLP组动脉环的收缩能力均有不同程度的恢复。结论 :败血症休克晚期VSM的低反应性可能涉及VSM细胞的钙稳态失调 ,NO的过量产生可能是导致这一变化的主要原因。AIM: To evaluate the alterations in calcium metabolism of the vascular smooth muscle in the late phase of septic shock and test the hypothesis that nitric oxide might be involved in sepsis-induced vascular hyporeactivity. METHODS: Male Sprague-Dawley rats were subjected to sepsis by cecal ligation and puncture (CLP). 18 hours post CLP,rat aortic rings were employed for measurement of contractile responses by using organ bath technique. RESULTS: In endothelium-denuded aortic rings from CLP rats,concentration-contraction curves to phenylephrine (PE) and KCl were significantly decreased when compared to that from sham control rats. The transient contraction induced by PE in calcium-free Krebs solution and the concentration-dependent contraction to CaCl_2 in KCl-depolarized medium were also markedly reduced. The hyporeactivity was partially reversed by treatment with aminoguanidine,a selective inducible nitric oxide synthase inhibitor. CONCLUSION: An impairment in calcium handling in vascular smooth muscle is involved in the vascular hyporeactivity during the late phase of septic shock,in which an excessive nitric oxide production might be the major mechanism.

关 键 词：脓毒症 主动脉 败血症休克 晚期 血管平滑肌 钙稳态 收缩反应 一氧化氮 

分 类 号：R631.3[医药卫生—外科学]