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地西泮可使清醒大鼠的反射性心动过缓加重。

Diazepam facilitates reflex bradycardia in conscious rats.

作者信息

Yang C P, Chou L S, Liu H J, Lin M T

机构信息

Department of Physiology, Taipei Medical College, Taiwan, ROC.

出版信息

J Pharm Pharmacol. 1987 Dec;39(12):1034-6. doi: 10.1111/j.2042-7158.1987.tb03156.x.

Abstract

The effects of diazepam on cardiovascular function were assessed in conscious rats. Intravenous administration of diazepam (1-30 mg kg-1) produced a dose-dependent decrease in both the mean arterial pressure and the heart rate. Also, reflex bradycardia was produced in rats by intravenous infusion of adrenaline (1.25-2.5 micrograms kg-1). Intravenous pretreatment of the rats with diazepam, although causing no change in the adrenaline-induced pressor effect, did enhance the adrenaline-induced reflex bradycardia. However, the diazepam enhancement of adrenaline-induced reflex bradycardia was antagonized by pretreatment of rats with an intravenous dose of picrotoxin (an agent blocks chloride channels by binding to sites associated with the benzodiazepine-GABA-chloride channel macromolecular complex). The data indicate that diazepam acts through the benzodiazepine-GABA-chloride channel macromolecular complex within the central nervous system to facilitate reflex bradycardia mediated through baroreceptor reflexes in response to an acute increase in arterial pressure.

摘要

在清醒大鼠中评估了地西泮对心血管功能的影响。静脉注射地西泮(1 - 30毫克/千克)可使平均动脉压和心率呈剂量依赖性下降。此外,静脉输注肾上腺素(1.25 - 2.5微克/千克)可使大鼠产生反射性心动过缓。地西泮对大鼠进行静脉预处理,虽然对肾上腺素引起的升压作用无影响,但确实增强了肾上腺素引起的反射性心动过缓。然而,静脉注射剂量的印防己毒素(一种通过与苯二氮卓 - γ - 氨基丁酸 - 氯化物通道大分子复合物相关位点结合来阻断氯离子通道的药物)对大鼠进行预处理后,可拮抗地西泮增强肾上腺素引起的反射性心动过缓的作用。数据表明,地西泮通过中枢神经系统内的苯二氮卓 - γ - 氨基丁酸 - 氯化物通道大分子复合物起作用,以促进在动脉压急性升高时通过压力感受器反射介导的反射性心动过缓。

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