外周血管阻力下降是感染性休克血压下降的关键因素之一。它可因各种舒血管物质释放增加所引起,亦可能与血管对缩血管物质的反应性下降有关。临床观察发现,感染性休克病人对去甲肾上腺素的反应减弱。体内、外动物实验也提示,感染性或内毒素性休克时,去甲肾上腺素的血管收缩效应减弱。感染性休克时血管对缩血管物质反应性减弱的机制目前仍不十分清楚。本实验复制大鼠腹膜炎休克模型,观察离体主动脉环对去甲肾上腺素反应性的变化,并分析血管内皮在血管反应性改变中可能具有的作用。材料与方法 Peripheral vascular resistance is one of the key factors in the decline of blood pressure in septic shock. It may be caused by an increase in the release of various vasodilators, and may also be related to decreased vasoconstrictor response. Clinical observations found that patients with septic shock response to norepinephrine weakened. In vivo and in vitro animal experiments also suggest that norepinephrine vasoconstriction is attenuated in infectious or endotoxic shock. The mechanism by which vasoconstrictor vasoconstrictors are attenuated during septic shock is still not fully understood. In this study, rat peritonitis shock model was duplicated to observe the change of noradrenaline responsiveness of isolated aorta rings and to analyze the possible role of vascular endothelial in vascular reactivity changes. Materials and Methods