Weinberger S E, Steinbrook R A, Carr D B, von Gal E R, Fisher J E, Leith D E, Fencl V, Rosenblatt M
J Appl Physiol (1985). 1985 May;58(5):1415-20. doi: 10.1152/jappl.1985.58.5.1415.
Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.
尽管给予阿片肽会抑制通气和通气反应性,但内源性阿片肽在调节通气反应性中的作用尚不清楚。我们通过将高碳酸血症反应性与免疫活性β-内啡肽的血浆水平相关联,并给予阿片拮抗剂纳洛酮,研究了12名成年男性志愿者体内内源性阿片类物质与通气反应之间的相互作用。纳洛酮预处理并未改变对高碳酸血症的通气反应性,仅此一点就表明内源性阿片类物质在调节这种反应中不起作用。然而,血浆中免疫活性β-内啡肽的基础水平与对CO2的通气反应性之间存在负相关关系。此外,短期高碳酸血症后血浆β-内啡肽水平升高,但仅在受试者预先用纳洛酮治疗时才会出现。我们得出结论,血浆内啡肽水平的测量表明内源性阿片肽与对CO2的通气反应之间存在关系,而这在仅限于评估纳洛酮作用的研究中并不明显。