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心力衰竭对交感神经活动压力反射控制的影响。

Effects of heart failure on baroreflex control of sympathetic neural activity.

作者信息

Ferguson D W, Berg W J, Roach P J, Oren R M, Mark A L

机构信息

Department of Internal Medicine, University of Iowa Hospitals, College of Medicine, Iowa City 52242.

出版信息

Am J Cardiol. 1992 Feb 15;69(5):523-31. doi: 10.1016/0002-9149(92)90998-e.

Abstract

Baroreflex control of heart rate, vascular resistance and norepinephrine is impaired in patients with heart failure, but recent animal studies demonstrate preserved baroreflex control of sympathetic nerve activity in this disorder. Studies were therefore performed to compare baroreflex control of efferent sympathetic nerve activity to muscle in 10 normal subjects (age mean +/- SEM 21 +/- 1 years) and in 11 patients with moderate to severe heart failure (age 48 +/- 5 years, New York Heart Association class II to IV, left ventricular ejection fraction 19 +/- 2%, pulmonary capillary wedge pressure 27 +/- 2 mm Hg, cardiac index 2.04 +/- 0.22 liters/min/m2). Baroreflex activation was produced by intravenous infusion of phenylephrine (0.5 to 2.0 micrograms/kg/min) and deactivation by infusion of nitroprusside (0.4 to 2.5 micrograms/kg/min). During phenylephrine infusion, comparable increases in mean arterial pressure were produced in normal subjects (89 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01) and in patients with heart failure (90 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01). The patients with heart failure exhibited significantly attenuated (p less than 0.01 for normal vs heart failure) decreases in heart rate (93 +/- 5 to 90 +/- 6 beats/min, p = not significant [NS]) compared with normal subjects (67 +/- 3 to 58 +/- 4 beats/min, p less than 0.01) and tended to demonstrate attenuated sympathoinhibitory responses to this pressor stimulus. More strikingly, patients with heart failure demonstrated significant impairment of baroreflex responses during nitroprusside-induced baroreceptor deactivation. In normal subjects, nitroprusside produced a decrease in mean arterial (90 +/- 2 to 80 +/- 3 mm Hg, p less than 0.001) and right atrial (4 +/- 1 to 2 +/- 1 mm Hg, p less than 0.01) pressures with a resultant reflex increase in heart rate (68 +/- 3 to 81 +/- 4 beats/min, p less than 0.001) and muscle sympathetic nerve activity (326 +/- 74 to 746 +/- 147 U/min, p less than 0.01). In patients with heart failure (n = 10), nitroprusside produced comparable (p = NS for normal vs heart failure) decreases in mean arterial (89 +/- 2 to 77 +/- 2 mm Hg, p less than 0.001) and right atrial (6 +/- 1 to 1 +/- 1 mm Hg, p less than 0.001) pressures, but did not significantly alter heart rate (91 +/- 6 to 97 +/- 4 beats/min, p = NS) or sympathetic nerve activity (936 +/- 155 to 1179 +/- 275 U/min, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

心力衰竭患者的压力反射对心率、血管阻力和去甲肾上腺素的控制受损,但最近的动物研究表明,在这种疾病中压力反射对交感神经活动的控制仍然存在。因此,我们进行了研究,以比较10名正常受试者(平均年龄±标准误21±1岁)和11名中重度心力衰竭患者(年龄48±5岁,纽约心脏协会II至IV级,左心室射血分数19±2%,肺毛细血管楔压27±2 mmHg,心脏指数2.04±0.22升/分钟/平方米)的压力反射对传出性交感神经活动至肌肉的控制情况。通过静脉输注去氧肾上腺素(0.5至2.0微克/千克/分钟)产生压力反射激活,通过输注硝普钠(0.4至2.5微克/千克/分钟)产生失活。在输注去氧肾上腺素期间,正常受试者(89±2至99±3 mmHg,p<0.01)和心力衰竭患者(90±2至99±3 mmHg,p<0.01)的平均动脉压有类似的升高。与正常受试者(67±3至58±4次/分钟,p<0.01)相比,心力衰竭患者心率下降幅度明显减弱(正常与心力衰竭相比p<0.01)(93±5至90±6次/分钟,p=无显著性差异[NS]),并且对这种升压刺激的交感抑制反应往往减弱。更引人注目的是,心力衰竭患者在硝普钠诱导的压力感受器失活期间表现出压力反射反应的显著受损。在正常受试者中,硝普钠使平均动脉压(90±2至80±3 mmHg,p<0.001)和右心房压(4±1至2±1 mmHg,p<0.01)下降,导致心率(68±3至81±4次/分钟,p<0.001)和肌肉交感神经活动(326±74至746±147 U/分钟)反射性增加(p<0.01)。在心力衰竭患者(n=10)中,硝普钠使平均动脉压(89±2至77±2 mmHg,p<0.001)和右心房压(6±1至1±1 mmHg,p<0.001)有类似的下降(正常与心力衰竭相比p=NS),但心率(91±6至97±4次/分钟,p=NS)或交感神经活动(936±155至1179±275 U/分钟,p=NS)没有显著改变。(摘要截断于400字)

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