败血症休克大鼠血浆肾上腺髓质素的变化

CHANGES OF PLASMA ADRENOMEDULLIN IN SEPTIC RATS

目的：探讨腹膜炎败血症休克大鼠血浆肾上腺髓质素（Ａｄｍ）的变化及其可能机制。方法：在ＳＤ大鼠用结扎盲肠和穿孔的方法复制大鼠腹膜炎败血症休克模型，术后９ｈ为早期败血症（ＥＳ），术后１８ｈ为晚期败血症（ＬＳ），放免测定主动脉孵育液和血浆Ａｄｍ。结果：早期败血症和晚期败血症大鼠（ｎ＝８）血浆Ａｄｍ分别增加５００％和２９０％（Ｐ＜０．０１），其主动脉释放Ａｄｍ分别增加１１０％（Ｐ＜０．０１）和２６．１％（Ｐ＜０．０５）。脂多糖（ＬＰＳ）（５～１０ｍｇ／Ｌ）、肾上腺素（ＥＰ，１０８ｍｏｌ／Ｌ）和内皮素１（ＥＴ１，１０９～１０７ｍｏｌ／Ｌ）均可浓度依赖性刺激正常主动脉释放Ａｄｍ增加。结论：败血症休克大鼠血浆Ａｄｍ在ＥＳ和ＬＳ均升高，血管释放Ａｄｍ受ＬＰＳ、ＥＴ１和ＥＰ等多种体液因素的调控。

Objective: To observe changes of plasma adrenomedullin(Adm) and its possible mechanisms in septic rats. Methods: Animal models of sepsis were made by cecum ligation and perforation. Adm release of vascular was observed by aortic incubation. Adm was measured by radioimmunoassay(RIA). Results: Plasma Adm of septic rats was increased by 500% and 290% in early sepsis (ES) and late sepsis (LS), respectively(P<0.01). Adm released by aorta of septic rats was increased by 110% and 26.1%(P<0.01). Lipopolysaccharide(LPS)(5～10 mg/L) , epinephrine (EP)(10~8 mol/L) and endotheline1(ET1)(10~9～10~7 mol/L) all dosedependently elevated Adm release from normal aorta. Conclusion: Plasma Adm increased in both ES and LS. Adm release from aorta was regulated by LPS, ET1 and EP.