依那普利拉增强心力衰竭患者交感神经活动的动脉和心肺压力反射控制。
Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure.
作者信息
Dibner-Dunlap M E, Smith M L, Kinugawa T, Thames M D
机构信息
Department of Medicine (Cardiology), University Hospitals of Cleveland, Case Western Reserve University, Cleveland, Ohio, USA.
出版信息
J Am Coll Cardiol. 1996 Feb;27(2):358-64. doi: 10.1016/0735-1097(95)00484-x.
OBJECTIVES
This study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activity.
BACKGROUND
Angiotensin-converting enzyme inhibitors decrease mortality in patients with congestive heart failure. Their efficacy appears to be related importantly to antiadrenergic effects, the mechanism for which has not been determined. Because baroreflexes tonically inhibit sympathetic outflow, and baroreflexes are blunted in heart failure, we hypothesized that these agents reduce sympathetic activity by augmenting baroreflexes.
METHODS
We assessed baroreflex control of sympathetic nerve activity and heart rate in patients with congestive heart failure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously). Arterial baroreflexes were perturbed by bolus administration of sodium nitroprusside and phenylephrine. Cardiopulmonary baroreflexes were perturbed by lower body negative pressure and head-down tilt. Muscle sympathetic nerve activity was recorded by microneurography.
RESULTS
Enalaprilat decreased systolic blood pressure in patients with heart failure and control subjects. Sympathetic nerve activity increased in control subjects but decreased in patients with heart failure after enalaprilat despite reductions in central venous pressure in this group. Baroreflex control of sympathetic nerve activity was unchanged by enalaprilat in control subjects. In patients with heart failure, both arterial and cardiopulmonary baroreflex control of sympathetic nerve activity was enhanced by enalaprilat. Baroreflex control of heart rate was unchanged by enalaprilat in either group.
CONCLUSIONS
Enalaprilat augments both arterial and cardiopulmonary baroreflex control of sympathetic activity in heart failure. These augmented inhibitory influences are associated with a reduction in sympathetic outflow and may contribute to the beneficial effects of angiotensin-converting enzyme inhibitors in heart failure.
目的
本研究旨在确定依那普利拉对交感神经活动反射控制的影响。
背景
血管紧张素转换酶抑制剂可降低充血性心力衰竭患者的死亡率。其疗效似乎与抗肾上腺素能作用密切相关，但其作用机制尚未明确。由于压力反射可抑制交感神经输出，且心力衰竭患者的压力反射减弱，我们推测这些药物通过增强压力反射来降低交感神经活动。
方法
我们评估了充血性心力衰竭患者和对照组在静脉注射依那普利拉（0.02mg/kg体重）前后交感神经活动和心率的压力反射控制情况。通过静脉注射硝普钠和去氧肾上腺素来干扰动脉压力反射。通过下体负压和头低位倾斜来干扰心肺压力反射。通过微神经电图记录肌肉交感神经活动。
结果
依那普利拉降低了心力衰竭患者和对照组的收缩压。依那普利拉给药后，对照组交感神经活动增加，而心力衰竭患者交感神经活动减少，尽管该组中心静脉压降低。依那普利拉对对照组交感神经活动的压力反射控制无影响。在心力衰竭患者中，依那普利拉增强了动脉和心肺对交感神经活动的压力反射控制。依那普利拉对两组患者的心率压力反射控制均无影响。
结论
依那普利拉增强了心力衰竭患者动脉和心肺对交感神经活动的压力反射控制。这些增强的抑制作用与交感神经输出减少有关，可能有助于血管紧张素转换酶抑制剂在心力衰竭中的有益作用。
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