Gahhos F N, Chiu R C, Hinchey E J, Richards G K
Arch Surg. 1982 Aug;117(8):1053-7. doi: 10.1001/archsurg.1982.01380320037010.
The pathophysiological role of endorphins in septic shock was studied in a porcine model. Septic shock was induced by the intravenous infusion of live Escherichia coli. Naloxone hydrochloride, an opiate receptor blocker, given during profound septic shock, increased blood concentrations of glucagon and cyclic adenosine monophosphate (cAMP), while BP and cardiac output increased transiently. Heart rate and hepatic glycogen value decreased, but insulin and cortisol levels remained unchanged. In contrast, exogenous morphine injection produced further reduction of BP, increased pulmonary wedge pressure, and increased substance P, while growth hormone level and cardiac output remained unchanged. Neither hormonal nor hemodynamic changes were noted in saline controls. Thus, the endogenous opiates appear partly responsible for the hemodynamic derangements during septic shock, and naloxone is able to reverse such depression, even though the effects are transient and relatively minor when naloxone is given late in the course of septic shock. Endogenous opiates also affect the hormonal homeostasis in shock, and there are indications that this may be mediated by the adenylate cyclase-cAMP system.
在内毒素休克的猪模型中研究了内啡肽的病理生理作用。通过静脉输注活的大肠杆菌诱导内毒素休克。在严重内毒素休克期间给予阿片受体阻滞剂盐酸纳洛酮，可增加胰高血糖素和环磷酸腺苷（cAMP）的血浓度，而血压和心输出量则短暂增加。心率和肝糖原值降低，但胰岛素和皮质醇水平保持不变。相比之下，注射外源性吗啡会使血压进一步降低，肺楔压升高，P物质增加，而生长激素水平和心输出量保持不变。在生理盐水对照组中未观察到激素或血流动力学变化。因此，内源性阿片类物质似乎部分导致了内毒素休克期间的血流动力学紊乱，并且纳洛酮能够逆转这种抑制作用，尽管在休克后期给予纳洛酮时效果是短暂且相对较小的。内源性阿片类物质也会影响休克时的激素稳态，并且有迹象表明这可能是由腺苷酸环化酶 - cAMP系统介导的。
