Gurll N
Adv Shock Res. 1983;10:63-71.
Naloxone has been used as a pharmacological tool to investigate the role of endorphins and opiate receptors in the cardiovascular pathophysiology of shock. It would appear that endorphins act on opiate receptors to contribute to the abnormalities found and that naloxone improves survival as well as cardiovascular function in shock. Preliminary studies in humans and the subhuman primate create cautious optimism regarding the clinical application of this information. Naloxone has served us well as a key to unlock the involvement of endorphins and opiate receptors in shock. However, further advances in our understanding may depend on the development and use of opiate receptor agonists and antagonists specific for the different opiate receptors described, each subserving different functions. Naloxone's disadvantage of increasing pain awareness may limit its clinical usefulness but might be overcome by using drugs that reverse the behavioral and neuroendocrine changes produced by beta-endorphin without altering pain relief. Thyrotropin-releasing hormone (TRH) is just such a "physiological" opiate antagonist which has been shown to increase MAP in experimental endotoxic and hemorrhagic shock [32].
纳洛酮已被用作一种药理学工具,以研究内啡肽和阿片受体在休克的心血管病理生理学中的作用。内啡肽似乎作用于阿片受体,从而导致所发现的异常情况,而纳洛酮可改善休克患者的生存率以及心血管功能。在人类和亚人类灵长类动物身上进行的初步研究,让人们对这一信息的临床应用产生了谨慎的乐观态度。纳洛酮作为一把钥匙,帮助我们了解了内啡肽和阿片受体在休克中的作用,对我们很有帮助。然而,我们理解的进一步进展可能取决于开发和使用针对所描述的不同阿片受体的阿片受体激动剂和拮抗剂,每种受体都有不同的功能。纳洛酮增加疼痛感知的缺点可能会限制其临床应用,但可以通过使用能逆转β-内啡肽产生的行为和神经内分泌变化而不改变疼痛缓解的药物来克服。促甲状腺激素释放激素(TRH)就是这样一种“生理性”阿片拮抗剂,已被证明可在实验性内毒素血症和失血性休克中提高平均动脉压[32]。