内啡肽和加压素在犬内毒素休克中的作用。

The role of endorphins and vasopressin in canine endotoxin shock.

作者信息

Cronenwett J L, Baver-Neff B S, Grekin R J, Sheagren J N

出版信息

J Surg Res. 1986 Dec;41(6):609-19. doi: 10.1016/0022-4804(86)90086-7.

Abstract

Chemical antagonists were used to assess the role of beta-endorphin and arginine-vasopressin (AVP) in canine endotoxin shock. Fifteen awake dogs were given Escherichia coli endotoxin IV. Within 5 min, CO decreased to 28%, LV dP/dt to 46%, and MAP to 52% baseline. Fifteen minutes after endotoxin, five dogs each received naloxone, AVP antagonist, or no treatment. Control (untreated) animals exhibited persistent cardiovascular depression, with CO 49%, LV dP/dt 69%, and MAP 91% of baseline after 45 min. Naloxone improved CO to 69%, LV dP/dt to 94%, and MAP to 91% by 30 min after treatment. AVP blockade improved CO to 105%, LV dP/dt to 107%, and MAP to 95% of baseline by 30 min after treatment, and caused significant tachycardia. Plasma cortisol and AVP increased markedly in all groups after endotoxin administration. AVP antagonist treatment increased mean survival from 1.4 to 4 days. These data suggest that abnormally elevated AVP contributes to cardiovascular depression in canine endotoxin shock and that AVP blockade is therapeutic in the animal model studied.

摘要

使用化学拮抗剂来评估β-内啡肽和精氨酸加压素（AVP）在犬内毒素休克中的作用。给15只清醒的犬静脉注射大肠杆菌内毒素。5分钟内，心输出量（CO）降至基线的28%，左心室dp/dt降至46%，平均动脉压（MAP）降至52%。内毒素注射15分钟后，每组5只犬分别接受纳洛酮、AVP拮抗剂治疗或不治疗。对照（未治疗）动物表现出持续性心血管抑制，45分钟后CO为基线的49%，左心室dp/dt为69%，MAP为91%。治疗后30分钟，纳洛酮使CO提高到69%，左心室dp/dt提高到94%，MAP提高到91%。AVP阻断使治疗后30分钟时CO提高到基线的105%，左心室dp/dt提高到107%，MAP提高到95%，并引起显著心动过速。内毒素给药后所有组血浆皮质醇和AVP均显著增加。AVP拮抗剂治疗使平均存活时间从1.4天延长至4天。这些数据表明，AVP异常升高导致犬内毒素休克时的心血管抑制，并且在本研究的动物模型中，AVP阻断具有治疗作用。