Lechner R B
Department of Anesthesiology, University of Virginia, Charlottesville 22908.
Circ Shock. 1992 Nov;38(3):157-64.
Naloxone potentiates the effects of adrenergic agonists when administered to hypovolemic dogs, and it has been assumed that this effect is due to naloxone's action at opiate receptors. To help determine the site and mechanism of this interaction, we administered naloxone and its "d" stereo-isomer (which does not bind to opiate receptors) to guinea pig papillary muscles in the presence and absence of pharmacologic (isoproterenol) and physiologic (treppe) inotropic stimulation. In control muscles and in rapidly paced muscles, naloxone was without significant inotropic effect. In the presence of isoproterenol, d- and l-naloxone exerted significant positive inotropic effects that were dose dependent. We conclude that, since both d- and l-naloxone potentiated the inotropic effects of isoproterenol and this was seen in the absence of opioids, naloxone may increase contractility by a nonopiate receptor-mediated mechanism.
给低血容量的狗注射纳洛酮时，它会增强肾上腺素能激动剂的作用，并且一直认为这种作用是由于纳洛酮作用于阿片受体所致。为了帮助确定这种相互作用的部位和机制，我们在有和没有药理学（异丙肾上腺素）和生理学（阶梯现象）变力刺激的情况下，给豚鼠乳头肌注射纳洛酮及其“d”立体异构体（它不与阿片受体结合）。在对照肌肉和快速起搏的肌肉中，纳洛酮没有显著的变力作用。在异丙肾上腺素存在的情况下，d - 纳洛酮和l - 纳洛酮都产生了显著的正性变力作用，且呈剂量依赖性。我们得出结论，由于d - 纳洛酮和l - 纳洛酮都增强了异丙肾上腺素的变力作用，并且这在没有阿片类药物的情况下也能看到，所以纳洛酮可能通过非阿片受体介导的机制增加收缩力。
