Role of adrenal medulla in hemodynamic response to hemorrhage and naloxone.

Role of adrenal medulla in hemodynamic response to hemorrhage and naloxone.
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肾上腺髓质在出血和纳洛酮的血流动力学反应中的作用。

DOI:
10.1152/ajpregu.1988.254.3.r559
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发表时间:
1988
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Gaddis,RR
Gaddis,RR
中科院分区:
--
文献类型:
--
作者:
Schadt,JC;Gaddis,RR

文献摘要

相似文献

我们测试了这样的假设:脑啡肽或肾上腺髓质在出血期间释放的一些其他化合物是导致低血压的原因。我们比较了完整兔、肾上腺去神经支配兔 (ADD) 和肾上腺切除兔 (ADX) 的血流动力学和血浆儿茶酚胺对出血和随后用纳洛酮阻断阿片受体的反应。这些研究是在有意识、长期准备的雄性新西兰白兔身上进行的。三组之间对出血的血流动力学反应没有差异。所有组的出血早期血浆去甲肾上腺素(NE)均升高。在ADD和ADX动物中,NE在向低血压转变时显着下降,表明周围交感神经释放的NE减少是压力下降的可能原因。在完整组中,NE 没有减少,而是达到一个平台,可能是由于肾上腺髓质释放了一些 NE,掩盖了交感神经释放的减少。尽管所有组中都存在对纳洛酮的升压反应,但肾上腺切除术或肾上腺去神经术减弱了纳洛酮的升压反应。所有组中纳洛酮的血浆 NE 反应相似,并且纳洛酮后血浆 NE 反应增加两到三倍。我们得出的结论是,脑啡肽或肾上腺释放的任何其他化合物与意识清醒的兔子出血期间的急性血流动力学变化无关。然而,肾上腺髓质释放的某些物质(可能是肾上腺素)确实在纳洛酮的升压作用中发挥作用,因为肾上腺切除术或去肾上腺神经可以降低纳洛酮的升压作用。
We tested the hypothesis that enkephalins or some other compound(s) released by the adrenal medulla during hemorrhage were responsible for the resultant hypotension. We compared the hemodynamic and plasma catecholamine responses to hemorrhage and subsequent opioid receptor blockade with naloxone in intact, adrenal-denervated (ADD), and adrenalectomized (ADX) rabbits. The studies were done in conscious, chronically prepared, male New Zealand White rabbits. The hemodynamic response to hemorrhage was not different among the three groups. Plasma norepinephrine (NE) increased early in hemorrhage in all groups. In the ADD and ADX animals, NE decreased significantly at the transition to hypotension, suggesting decreased release of NE by peripheral sympathetic nerves as a possible cause of the decrease in pressure. In the intact group, NE did not decrease but reached a plateau possibly due to the release of some NE by the adrenal medulla, which obscured the decreased release by sympathetic nerves. The pressor response to naloxone, though present in all groups, was attenuated by adrenalectomy or adrenal denervation. The plasma NE response to naloxone was similar in all groups and involved a two- to threefold increase after naloxone. We conclude that enkephalins or any other compounds released by the adrenal gland are not responsible for the acute hemodynamic changes during hemorrhage in the conscious rabbit. However, some substance(s) released by the adrenal medulla, perhaps epinephrine, does play a role in naloxone's pressor effect, since this is reduced by adrenalectomy or adrenal denervation.