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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,108mol/L)和内皮素1(ET1,109~107mol/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、ET1和EP等多种体液因素的调控。
Objective: To investigate the changes of plasma adrenomedullin (Adm) and its possible mechanism in rats with peritonitis and septicemia. Methods: The rat model of peritonitis and septicemia was established by ligating cecal and perforation in SD rats. Early post-sepsis (ES) was performed at 9 hours and late sepsis (LS) at 18 hours after operation. Radioimmunoassay was used to determine the aorta and plasma Adm . Results: The plasma Adm in early septicemia and late sepsis rats (n = 8) increased by 500% and 290%, respectively (P <0.01), and the release of Adm in the aorta increased by 110% (P <0.01) 1% (P <0.05). Lipopolysaccharide (LPS) (5 ~ 10mg / L), epinephrine (EP, 10 8mol / L) and endothelin 1 (ET 1,109 ~ 10 7mol / L) can be concentration-dependent stimulation Normal aorta release increased Adm. CONCLUSIONS: The plasma Adm is increased in both ES and LS in septic shock rats. The release of Adm from blood vessels is regulated by many humoral factors such as LPS, ET-1 and EP.