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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。
This article explored the role of three regulatory peptides in the pathogenesis of shock. The results showed that: (1) plasma endothelin (ET) in septic shock rats increased exponentially, and continuous infusion of low-dose ET to healthy rats could result in significant shock performance, while intravenous infusion of ET to mild hemorrhagic shock rats Induced irreversible shock, with specific ET-antiserum treatment of shock, with significant effect; (2) plasma calcitonin gene-related peptide (CGRP) increased 2.6-fold in septic shock rats, shock early or late treatment with low-dose CGRP have (3) The levels of angiotensin Ⅱ in the myocardium and aorta of shock rats were significantly increased, and the early suppression of shock increased the severity of shock and the later inhibited the increase of angiotensin Ⅱ Conclusion: ET is involved in the pathogenesis of shock Body fluid factors, CGRP participate in the body’s compensatory regulation of shock, tissue angiotensin II in different stages of shock in different roles.