Alterations in the baroreceptor reflex in conscious dogs with heart failure.

Alterations in the baroreceptor reflex in conscious dogs with heart failure.
复制标题

患有心力衰竭的意识清醒的狗的压力感受器反射的改变。

DOI:
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发表时间:
1972
影响因子:
15.9
通讯作者:
E. Braunwald
E. Braunwald
中科院分区:
医学1区
文献类型:
--
作者:
C. Higgins;S. Vatner;D. Eckberg;E. Braunwald

文献摘要

被引文献

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本文比较了压力感受性反射对实验性心肌肥厚和心力衰竭清醒犬与正常清醒犬的作用。三尖瓣撕脱和进行性肺动脉瓣狭窄可导致心肌肥厚和心力衰竭。压力感受器反射对短暂性高血压的敏感性通过确定回归线的斜率来评估,回归线将R-R间期的延长与静脉注射1-苯肾上腺素引起的动脉压短暂升高期间收缩期动脉压的升高相关联。16只正常动物的平均斜率平均为22.4+/-2.3 msec/nm Hg。23.1在5只假手术动物中显著降低至8.3 +/-0.8(P < 0.001),在9只心力衰竭犬中显著降低至3.3+/-0.5(P < 0.001)。在6只正常和6只心力衰竭犬的双侧颈动脉闭塞(BCO)过程中,比较了压力感受性低血压的反应,这些犬先前在肠系膜上级动脉和肾动脉上装有多普勒血流传感器。在BCO期间,正常犬的动脉压增加52+/-4 mm Hg,心率增加33+/-2次/min,肠系膜阻力增加0.17+/-0.03 mm Hg/ml/min,肾阻力增加0.37+/-0.10 mm Hg/ml/min。在心力衰竭组,所有这些变量的增加均显著较少(P < 0.01);动脉压升高25 ± 3 mm Hg,心率13 ± 4次/min,肠系膜阻力0.04 ± 0.007 mm Hg/ml/min,肾阻力0.18 ± 0.09 mm Hg/ml/min。因此,在心力衰竭中,压力感受器低血压和高血压引起的所有测量的全身和局部循环调节都明显减弱。这项研究表明,在实验性心力衰竭的一个主要的心血管控制机制的深刻紊乱。
The effectiveness of the baroreceptor reflex in conscious dogs with experimental cardiac hypertrophy and heart failure was compared with that in a group of normal conscious dogs. Cardiac hypertrophy and heart failure were produced by tricuspid avulsion and progressive pulmonary stenosis. The sensitivity of the baroreceptor reflex to transient hypertension was assessed by determining the slope of the regression line relating the prolongation of the R-R interval to the rise in systolic arterial pressure during the transient elevation of arterial pressure induced by an intravenous injection of 1-phenylephrine. The mean slope averaged 22.4+/-2.3 msec/nm Hg in 16 normal animals. 23.1 +/-1.5 in five sham-operated animals, and was significantly reduced to 8.3 +/-0.8 in 10 dogs with hypertrophy alone (P < 0.001), and to 3.3+/-0.5 in nine dogs with heart failure (P < 0.001). The response to baroreceptor hypotension was compared during bilateral carotid artery occlusion (BCO) in six normal and six heart failure dogs previously instrumented with Doppler flow transducers on the superior mesenteric and renal arteries. During BCO, in normal dogs arterial pressure increased 52+/-4 mm Hg, heart rate 33+/-2 beats/min, mesenteric resistance 0.17+/-0.03 mm Hg/ml per min, and renal resistance 0.37+/-0.10 mm Hg/ml per min. In the heart failure group all of these variables increased significantly less (P < 0.01); arterial pressure rose 25 +/-3 mm Hg, heart rate 13 +/-4 beats/min, mesenteric resistance 0.04+/-0.007 mm Hg/ml per min, and renal resistance 0.18+/-0.09 mm Hg/ml per min.Thus, in heart failure, all measured systemic and regional circulatory adjustments consequent to baroreceptor hypo- and hypertension are markedly attenuated. This study demonstrates a profound derangement of a major cardiovascular control mechanism in experimental heart failure.