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纳洛酮未能降低原发性高血压患者中可乐定引起的血压降低及血浆去甲肾上腺素水平。

Failure of naloxone to reduce the clonidine induced reduction of blood pressure and plasma noradrenaline in patients with essential hypertension.

作者信息

Bramnert M, Hökfelt B

出版信息

Acta Physiol Scand. 1983 Aug;118(4):379-83. doi: 10.1111/j.1748-1716.1983.tb07287.x.

Abstract

Studies in animals and man indicate a functional interaction between the adrenergic and the opiate systems. In the present study the effect of the opiate receptor blocker naloxone on the reduction of blood pressure and plasma noradrenaline induced by the alpha 2-agonist clonidine was investigated in nine patients with essential hypertension. In a randomised manner the patients received a bolus dose of naloxone (10 micrograms/kg) or physiological saline followed by a slow infusion of naloxone (5 micrograms/kg/h) or saline, respectively. Fifteen minutes after the respective bolus dose, clonidine (3 micrograms/kg) was infused over 10 minutes. Naloxone had no effect on the clonidine induced hypotension and reduction of plasma noradrenaline. Accordingly, there is no evidence that the clonidine induced reduction of blood pressure and plasma noradrenaline involves opiate receptors that can be blocked by naloxone. Plasma adrenaline increased significantly during the early phase of naloxone infusion.

摘要

对动物和人类的研究表明,肾上腺素能系统与阿片系统之间存在功能相互作用。在本研究中,对9名原发性高血压患者研究了阿片受体阻滞剂纳洛酮对α2-激动剂可乐定诱导的血压降低和血浆去甲肾上腺素减少的影响。患者以随机方式接受一剂推注纳洛酮(10微克/千克)或生理盐水,随后分别缓慢输注纳洛酮(5微克/千克/小时)或生理盐水。在各自推注剂量15分钟后,在10分钟内输注可乐定(3微克/千克)。纳洛酮对可乐定诱导的低血压和血浆去甲肾上腺素减少没有影响。因此,没有证据表明可乐定诱导的血压和血浆去甲肾上腺素降低涉及可被纳洛酮阻断的阿片受体。在纳洛酮输注的早期阶段,血浆肾上腺素显著增加。

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