Effect of experimental heart failure on peripheral sympathetic vasoconstriction.

Effect of experimental heart failure on peripheral sympathetic vasoconstriction.
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实验性心力衰竭对周围交感血管收缩的影响。

DOI:
10.1152/ajpheart.1988.254.4.h727
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发表时间:
1988
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Ferraro,N
Ferraro,N
中科院分区:
--
文献类型:
--
作者:
Wilson,JR;Matthai,W;Lanoce,V;Frey,M;Ferraro,N

文献摘要

被引文献

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为探讨心力衰竭是否损害外周交感血管收缩,在正常犬和快速心室起搏所致慢性心力衰竭犬中,观察了后肢血管对腰链刺激(0.5~20赫兹)的反应。腰链刺激率在0.5~3赫兹时,两组后肢血管反应相似。然而,在5-20赫兹的刺激率下,心力衰竭犬的血管反应明显减弱。血管对去甲肾上腺素(0.1、1和10微克/分钟)的反应没有改变。这些发现表明,慢性心力衰竭导致交感神经血管收缩受损,可能是因为神经递质释放减少。这种异常可能会干扰衰竭的循环补偿低心输出量的能力,从而加剧心力衰竭的严重程度。
To investigate whether heart failure impairs peripheral sympathetic vasoconstriction, hindlimb vascular responses to lumbar chain stimulation (0.5-20 Hz) were studied in normal dogs and in dogs with chronic heart failure produced by rapid ventricular pacing. At lumbar chain stimulation rates of 0.5-3 Hz, hindlimb vascular responses were comparable in both groups. However, at stimulation rates of 5-20 Hz, vascular responses were significantly attenuated in the dogs with heart failure. Vascular responses to norepinephrine (0.1, 1, and 10 micrograms/min) were not altered. These findings suggest that chronic heart failure results in impaired sympathetic vasoconstriction, probably because of reduced neurotransmitter release. This abnormality may interfere with the capacity of the failing circulation to compensate for a low cardiac output and thereby intensify the severity of heart failure.