【摘要】 在大鼠盲肠结扎加穿孔造成的腹膜炎败血症休克模型上发现,心肌肌膜Na⁺—K⁺—ATP酶活性呈双时相变化。早期休克时,Na⁺—K⁺—ATP酶活性比对照组高48％（P<0.01）,晚期休克时比时照组低42％（P<0.01）。心肌肌膜哇巴因结合位点数目和磷酸化位点数目也呈早期增加（P<0.01）,晚期降低（P<0.01）双时相变化。离体心脏灌流发现,败血症休克大鼠心脏的收缩功能也呈早期增强,晚期减弱的双时相变化,而心脏对灌流硅巴因(10^-7～10^-5mol/L)的反应性亦呈早期增加,晚期降低。结果提示,腹膜炎败血症休克时心脏收缩功能的改变与大鼠心肌肌膜Na⁺—K⁺—ATP酶变化有关。更多还原

【Abstract】 On rat peritonitis induced by cecal ligation and puncture, it was found that cardiac sarcolemma Na +-K+- ATPase activity was a biphasic process in which Na +- K+- ATPase was increased by 48% (P< 0.01) during early sepsis (ES) and decreased by 42%(P<0.01) during late sepsis (LS). The numbers of ouabain binding sites and phosphorylation sites were increased(P<0.01) in ES and decreased (P<0.01) in LS. It was found in isolated perfused rat hearts that contractile function of the septic rat hearts was strengthened during ES and weakened during LS. Responsiveness of isolated perfused rat hearts to 10-7～10-5mol/L ouabain was enhanced in ES and reduced in LS. These data suggested that changes of contractile function of septic hearts relate to changes of myocardial Na +-K+- ATPase.更多还原