Naloxone reversal of hypovolemic shock in dogs.
Naloxone reversal of hypovolemic shock in dogs.
复制标题
纳洛酮逆转狗低血容量休克。
DOI：
10.1097/00132586-198106000-00003
复制
发表时间：
1981
期刊：
影响因子：
--
通讯作者：
A. Faden
中科院分区：
文献类型：
--
作者：
T. Vargish;D. Reynolds;N. Gurll;R. Lechner;J. Holaday;A. Faden
内源性阿片配体β-内啡肽在应激时释放。我们使用阿片受体阻断剂纳洛酮来验证内啡肽可能参与失血性休克病理生理的假设。将两组5只麻醉的狗装备成仪器以监测心血管性能，并使它们经受如下方案：将它们流血的到储血器中以将平均动脉压降低至45 mmHg并在该压力下维持1小时。此时，夹闭储药器，一组犬接受纳洛酮（2 mg/kg）静脉推注和2 mg/kg-hr输注。这些犬表现出动脉压、左心室dp/dtmax和心输出量的迅速增加。在t = 2小时时返回流出的血液，并继续药物输注2小时。对照组犬接受等体积生理盐水。对照组犬在夹闭储药器后30分钟内死亡，而所有5只治疗组犬均存活超过72小时（P <0.02）。这些数据表明内啡肽作用于阿片受体参与了休克模型的病理生理过程。
The endogenous opiate ligand, beta-endorphin, is released during stress. We tested the hypothesis that endorphins may be involved in the pathophysiology of hemorrhagic shock by using the opiate receptor blocking agent, naloxone. Two groups of five anesthetized dogs were instrumented to monitor cardiovascular performance and subjected to a protocol in which they were bled into a reservoir to lower mean arterial pressure to 45 mmHg and maintained at that pressure for one hour. At that time the reservoir was clamped and on group of dogs received an intravenous bolus of naloxone (2 mg/kg) and an infusion at 2 mg/kg-hr. These dogs demonstrated a prompt increase in arterial pressure, left ventricular dp/dtmax and cardiac output. The shed blood was returned at t = 2 hr and drug infusion continued for 2 hours. The control group of dogs received saline in equivalent volume. The control dogs died within 30 minutes of clamping the reservoir while all five treated dogs survived beyond 72 hours (P less than 0.02). These data suggest the involvement of endorphins acting on opiate receptors as part of the pathophysiology in this shock model.