血管扩张剂治疗高血压期间反射性心脏刺激的交感和副交感成分。

A J Man in 't Veld, G J Wenting, R P Verhoeven, M A Schalekamp
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引用次数: 6

摘要

1. 研究了15例高血压患者每日应用320 mg心得安阻断慢性肾上腺素受体前后,静脉注射300 mg二氮氧化物的血流动力学反应。单独使用二氮唑后,平均动脉压和总外周阻力分别降低24 +/- 3%和35 +/- 5%(平均+/- SEM)。心输出量和心率分别上升了25 +/- 9%和21 +/- 3%。在β -肾上腺素受体阻断期间,血管舒张后平均动脉压、心率、心输出量和总外周阻力的百分比变化与单独使用二氮氧化合物后无显著差异。2. 对12例长期接受β -肾上腺素受体阻断治疗的高血压患者,在二氮氧化合物急性血管扩张治疗前给予0.04 mg/kg体重的阿托品。肾上腺素受体联合副交感神经阻滞后,二氮氧化物未引起心率增加。然而,心输出量增加了14±5%。3.我们得出结论,副交感神经张力的戒断是β -肾上腺素受体阻断期间急性血管舒张后循环稳态的重要决定因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sympathetic and parasympathetic components of reflex cardiostimulation during vasodilator treatment of hypertension.

1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic beta-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 +/- 3 and 35 +/- 5% (mean +/- SEM) respectively. Cardiac output and heart rate rose by 25 +/- 9 and 21 +/- 3%. During beta-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0.04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with beta-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined beta-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 +/- 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during beta-adrenoreceptor blockade.

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