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肾上腺髓质中的多巴胺能受体可能是氟哌利多诱发高血压反应的作用位点。

A dopaminergic receptor in adrenal medulla as a possible site of action for the droperidol-evoked hypertensive response.

作者信息

Montiel C, Artalejo A R, Bermejo P M, Sánchez-García P

出版信息

Anesthesiology. 1986 Nov;65(5):474-9. doi: 10.1097/00000542-198611000-00004.

DOI:10.1097/00000542-198611000-00004
PMID:3777477
Abstract

Recently, an inhibitory dopaminergic receptor has been described that modulates catecholamine release from adrenal medulla. It has also been reported that low doses of droperidol increase arterial pressure in some patients with pheochromocytoma. The authors investigated whether an effect of droperidol on such a receptor could be one of the mechanisms involved in the hypertensive response. Isolated cat adrenal glands were perfused with Krebs-bicarbonate solution, and the catecholamine release was measured in the effluent. Then, the glands were stimulated by activation of the nicotinic receptor (nicotine, 5 microM), and the effect of low and high doses of droperidol and/or apomorphine on the catecholamine secretory responses evoked by nicotine was investigated. Low concentrations of droperidol (0.05 microM) (a dopaminergic antagonist) markedly increased the secretory response induced by nicotine whereas higher concentrations (50 microM) decreased it. Apomorphine (1 microM) (a dopaminergic agonist) inhibits the catecholamine release produced by nicotine, and this inhibitory effect was completely reversed by the lowest concentration of droperidol but not by the highest. In fact, the high concentration of droperidol further inhibited the catecholamine release induced by nicotine. The results suggest that the hypertensive responses evoked by low doses of droperidol in some patients with pheochromocytoma could be due to the inactivation of a dopaminergic inhibitory system present in the adrenal medulla that, under physiologic conditions, limits the amount of catecholamines released by the gland. Such as an inhibitory mechanism could operate in an exaggerated manner in patients with pheochromocytoma.

摘要

最近,已描述了一种抑制性多巴胺能受体,它可调节肾上腺髓质儿茶酚胺的释放。也有报道称,低剂量氟哌利多可使一些嗜铬细胞瘤患者的动脉血压升高。作者研究了氟哌利多对这种受体的作用是否可能是高血压反应所涉及的机制之一。用 Krebs - 碳酸氢盐溶液灌注离体猫肾上腺,并测量流出液中的儿茶酚胺释放量。然后,通过激活烟碱样受体(尼古丁,5 microM)刺激肾上腺,研究低剂量和高剂量氟哌利多和/或阿扑吗啡对尼古丁诱发的儿茶酚胺分泌反应的影响。低浓度氟哌利多(0.05 microM)(一种多巴胺能拮抗剂)显著增加尼古丁诱导的分泌反应,而较高浓度(50 microM)则使其降低。阿扑吗啡(1 microM)(一种多巴胺能激动剂)抑制尼古丁产生的儿茶酚胺释放,且这种抑制作用可被最低浓度的氟哌利多完全逆转,但不能被最高浓度逆转。实际上,高浓度氟哌利多进一步抑制尼古丁诱导的儿茶酚胺释放。结果表明,低剂量氟哌利多在一些嗜铬细胞瘤患者中诱发的高血压反应可能是由于肾上腺髓质中存在的多巴胺能抑制系统失活所致,在生理条件下,该系统可限制肾上腺释放的儿茶酚胺量。这种抑制机制在嗜铬细胞瘤患者中可能会过度发挥作用。

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Adverse drug reactions in patients with phaeochromocytoma: incidence, prevention and management.
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Anaesthesia for phaeochromocytoma.嗜铬细胞瘤的麻醉
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