Role of Regulatory Peptide in Pathogenesis of Shock

The present study evaluated the pathogenetic roles of three kinds of regulatory peptide. The results showed that (i) plasma endothelin(ET) level elevated significantly in septic shock rats, persistent intravenous drip of low doses ET caused development of shock state in normal rats and the irreversible outcome of light hemorrhagic shock. Furthermore, i. v. administration of specific ET-antiserum was significantly effective to septic shock rats, (Ⅱ) Plasma calcitonin gene-related peptide (CGRP) increased by 260% in septic shock rats, i. v. drip of low doses CGRP both in early and late sepsis were effective to shock rats, (Ⅱi) An-giotensin-Ⅱ (ANG-Ⅱ) contents of heart and aorta increased dramatically both in early and late septic shock, and inhibiting its increase with Captopril in late sepsis significantly improved the shock state, but results were inverse in early sepsis. It could be concluded that ET was one of the most important factors participating in the pathogenesis of shock, CGRP had a compens     

调节肽在休克发病中的作用

本文探讨了三种调节肽在休克发病中的作用。结果表明:(1)败血症休克大鼠血浆内皮素(ET)成倍增加,给健康大鼠持续滴注低剂量ET可致明显的休克表现,而给轻度失血休克大鼠静滴ET,则致休克不可逆,用特异的ET-抗血清治疗休克,具有明显疗效;(2)败血症休克大鼠血浆降钙素基因相关肽(CGRP)增加2.6倍,休克早期或晚期运用低剂量CGRP治疗都具有显著疗效;(3)休克大鼠心肌、主动脉组织血管紧张素Ⅱ明显增加,休克早期抑制其增加可加剧休克,晚期抑制其升高则具有显著疗效.结论认为,ET是参与休克发病的重要体液因素,CGRP参与休克时机体的代偿调节,组织血管紧张素Ⅱ在休克不同时期作用不同。