Dibner-Dunlap M E, Thames M D
Department of Internal Medicine, Medical College of Virginia/Virginia Commonwealth University, Richmond.
Circ Res. 1989 Dec;65(6):1526-35. doi: 10.1161/01.res.65.6.1526.
The purpose of this study was to determine if arterial baroreflex control of sympathetic nerve traffic is impaired in heart failure. We recorded renal nerve activity during changes in arterial pressure while simultaneously recording from aortic baroreceptor afferent fibers in 10 dogs with heart failure induced by rapid ventricular pacing and in 10 sham animals. Sensitivity of the aortic baroreceptors (percent change in nerve activity per millimeters mercury change in mean arterial pressure) was reduced in the heart failure group (heart failure, 2.3 +/- 0.3; sham, 3.6 +/- 0.4, p = 0.02). Despite the reduced sensitivity of aortic baroreceptors in heart failure, there was no difference in the baroreflex gain of renal nerve activity (heart failure, -5.5 +/- 1.4; sham, -5.8 +/- 1.3, p = NS). These values tended to decrease in both groups after vagotomy. The relation between baroreceptor input and renal sympathetic output, or central baroreflex gain (percent change in renal nerve activity divided by percent change in aortic nerve activity) was similar in both groups before vagotomy (heart failure, -2.4 +/- 0.6; sham, -2.3 +/- 0.5, p = NS). Vagotomy reduced central gain in the sham group (-0.9 +/- 0.1, p = 0.03) but not in the heart failure group (-1.7 +/- 0.5, p = NS), suggesting that the contribution of vagal afferents in the baroreflex arc is reduced in heart failure. Baroreflex control of R-R interval was attenuated in heart failure when assessed by blood pressure elevation but not reduction, indicating abnormal parasympathetic but preserved cardiac sympathetic mechanisms in heart failure. Thus, dogs with heart failure exhibit reduced sensitivity of aortic baroreceptors but preserved baroreflex control of renal nerve activity. Reduced baroreceptor sensitivity with preservation of baroreflex control of sympathetic nerve activity may contribute to the sympathoexcitatory state known to exist in heart failure.
本研究的目的是确定心力衰竭时动脉压力感受器对交感神经活动的控制是否受损。我们在10只通过快速心室起搏诱导心力衰竭的犬和10只假手术动物中，记录动脉压变化期间的肾神经活动，同时记录主动脉压力感受器传入纤维的活动。心力衰竭组主动脉压力感受器的敏感性（平均动脉压每变化1毫米汞柱时神经活动的百分比变化）降低（心力衰竭组为2.3±0.3；假手术组为3.6±0.4，p = 0.02）。尽管心力衰竭时主动脉压力感受器的敏感性降低，但肾神经活动的压力反射增益并无差异（心力衰竭组为-5.5±1.4；假手术组为-5.8±1.3，p =无显著性差异）。迷走神经切断术后，两组的这些值均有下降趋势。在迷走神经切断术前，两组压力感受器传入与肾交感输出之间的关系，即中枢压力反射增益（肾神经活动的百分比变化除以主动脉神经活动的百分比变化）相似（心力衰竭组为-2.4±0.6；假手术组为-2.3±0.5，p =无显著性差异）。迷走神经切断术使假手术组的中枢增益降低（-0.9±0.1，p = 0.03），但心力衰竭组未降低（-1.7±0.5，p =无显著性差异），这表明心力衰竭时迷走神经传入在压力反射弧中的作用减弱。当通过血压升高而非降低来评估时，心力衰竭时压力反射对R-R间期的控制减弱，表明心力衰竭时副交感神经机制异常但心脏交感神经机制保留。因此，心力衰竭犬表现出主动脉压力感受器敏感性降低，但压力反射对肾神经活动的控制保留。压力感受器敏感性降低而交感神经活动的压力反射控制保留，可能导致心力衰竭中已知存在的交感神经兴奋状态。
