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在心力衰竭中,迷走神经机械反射对交感神经活动的控制作用减弱。

Control of sympathetic nerve activity by vagal mechanoreflexes is blunted in heart failure.

作者信息

Dibner-Dunlap M E, Thames M D

机构信息

Department of Medicine, University Hospitals of Cleveland, Case Western Reserve University, Ohio.

出版信息

Circulation. 1992 Dec;86(6):1929-34. doi: 10.1161/01.cir.86.6.1929.

Abstract

BACKGROUND

Previous studies have documented abnormalities of arterial baroreflexes in animals and patients with congestive heart failure. This study determined whether cardiopulmonary reflex control of sympathetic nerve activity was abnormal in a canine model of low-output heart failure induced by rapid ventricular pacing.

METHODS AND RESULTS

We stimulated mechanoreceptors throughout the cardiopulmonary region by volume expansion and left atrial mechanoreceptors selectively by inflating small balloons at the junctions of the pulmonary veins and left atrium. Responses of renal sympathetic nerve activity and left atrial and systemic arterial pressures were recorded. In the control group, 15% volume expansion raised left atrial pressure 3.5 +/- 0.8 mm Hg and resulted in a 70 +/- 8% reduction in renal nerve activity. In the heart failure group, 15% volume expansion resulted in a 6.8 +/- 3.0 mm Hg rise in left atrial pressure with only a 16 +/- 20% reduction in renal nerve activity (p < 0.01). When volume expansion was performed after pretreatment with hemorrhage to lower left atrial pressure to the normal range in the heart failure group, the markedly attenuated response in the heart failure group persisted. After vagotomy, volume expansion elicited no change in renal nerve activity. Inflation of the atrial balloons caused a 28 +/- 9% reduction in renal sympathetic nerve activity and a 13 +/- 4 mm Hg decrease in arterial pressure in the control group. Renal nerve activity (-5 +/- 3%) and mean arterial pressure (-1 +/- 1 mm Hg) did not change with balloon inflation in the heart failure group.

CONCLUSIONS

We conclude that dogs with low-output heart failure exhibit marked attenuation of cardiopulmonary mechanoreflex control of sympathetic nerve activity. This attenuated response is mediated via cardiac vagal afferent fibers and is due to either abnormalities in cardiopulmonary baroreceptors or abnormalities in the central nervous system.

摘要

背景

先前的研究已证明充血性心力衰竭动物和患者存在动脉压力反射异常。本研究旨在确定在快速心室起搏诱导的低输出量心力衰竭犬模型中,交感神经活动的心肺反射控制是否异常。

方法与结果

我们通过容量扩张刺激整个心肺区域的机械感受器,并通过在肺静脉与左心房交界处充气小气球选择性刺激左心房机械感受器。记录肾交感神经活动以及左心房和体动脉压力的反应。在对照组中,15%的容量扩张使左心房压力升高3.5±0.8 mmHg,并导致肾神经活动降低70±8%。在心力衰竭组中,15%的容量扩张使左心房压力升高6.8±3.0 mmHg,而肾神经活动仅降低16±20%(p<0.01)。当在心力衰竭组中通过出血预处理使左心房压力降至正常范围后再进行容量扩张时,心力衰竭组中明显减弱的反应仍然存在。迷走神经切断术后,容量扩张未引起肾神经活动变化。在对照组中,心房气球充气使肾交感神经活动降低28±9%,动脉压力降低13±4 mmHg。在心力衰竭组中,气球充气后肾神经活动(-5±3%)和平均动脉压(-1±1 mmHg)未发生变化。

结论

我们得出结论,低输出量心力衰竭犬表现出心肺机械反射对交感神经活动的明显减弱。这种减弱的反应是通过心脏迷走传入纤维介导的,并且是由于心肺压力感受器异常或中枢神经系统异常所致。

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