Koskinen L O
Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Peptides. 1991 Nov-Dec;12(6):1273-7. doi: 10.1016/0196-9781(91)90206-5.
The cardiovascular effects of IV naloxone and a subsequent administration of TRH IV were studied in the rabbit. Naloxone caused a vasodilation in the myocardium and adrenal glands. Naloxone elicited an increment in cerebral blood flow in several regions which attenuated the cerebrovasodilating effect of TRH in a few regions. The blockade of endogenous opioids with naloxone did not modify the peripheral vasoconstricting effect of TRH or affect the vascular effects of TRH mediated by the peripheral sympathetic nerves. The results indicate that naloxone has a vasodilating effect in the myocardium and CNS in anesthetized rabbits. The major part of the cardiovascular effect of TRH is not dependent on mechanisms sensitive to naloxone.
在兔子身上研究了静脉注射纳洛酮及随后静脉注射促甲状腺激素释放激素(TRH)的心血管效应。纳洛酮可引起心肌和肾上腺血管舒张。纳洛酮使几个脑区的脑血流量增加,这减弱了TRH在少数脑区的脑血管舒张作用。用纳洛酮阻断内源性阿片类物质并未改变TRH的外周血管收缩作用,也未影响外周交感神经介导的TRH的血管效应。结果表明,纳洛酮对麻醉兔的心肌和中枢神经系统有血管舒张作用。TRH心血管效应的主要部分不依赖于对纳洛酮敏感的机制。