Sanders J S, Ferguson D W, Mark A L
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
Circulation. 1988 Feb;77(2):279-88. doi: 10.1161/01.cir.77.2.279.
Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation of arterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 +/- 2.8 to 94.9 +/- 2.9 mm Hg (+/- SE, p less than .001). This was accompanied by a decrease in heart rate from 65.8 +/- 3.4 to 56.1 +/- 3.3 beats/min (p less than .001) and a decrease in MSNA from 236.2 +/- 47.5 to 84.5 +/- 19.3 units (p less than .001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 +/- 2.9 mm Hg (p less than .001 versus control or PE alone), and heart rate returned to control levels of 62.9 +/- 2.0 beats/min (p = NS vs control; p less than .01 PE vs PE plus NP), but MSNA remained reduced at 48.6 +/- 9.2 units (p less than .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 +/- 5% attenution of MSNA, while activation of ABR alone resulted in a 73 +/- 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.(ABSTRACT TRUNCATED AT 400 WORDS)
颈动脉窦（CBR）和主动脉弓（ABR）区域的动脉压力感受器对心率以及外周血管对动脉压变化的反应发挥着重要的控制作用。在人体动脉压持续升高期间，这两条压力反射通路在控制交感神经活动方面的相对作用尚不清楚。因此，我们研究了在正常人类受试者动脉压升高期间，颈动脉与主动脉压力反射对肌肉交感神经活动（MSNA）控制的相对贡献。在8名正常男性（第一组）中，我们测量了单独静脉输注去氧肾上腺素（PE）使动脉压持续升高时（联合激活ABR和CBR）的MSNA（微神经ography），以及在PE输注期间叠加持续的颈部外部压力（NP）时的MSNA。在持续输注PE期间施加NP，以消除跨壁颈动脉窦压力的升高，从而消除CBR激活，进而仅引起ABR刺激。直接测量平均动脉压，在输注PE期间保持中心静脉压恒定，并将MSNA测量为总活动（爆发频率×幅度），并以单位表示。输注PE（激活ABR和CBR）使平均动脉压从87.2±2.8 mmHg升高至94.9±2.9 mmHg（±SE，p<0.001）。这伴随着心率从每分钟65.8±3.4次降至56.1±3.3次（p<0.001），以及MSNA从236.2±47.5单位降至84.5±19.3单位（p<0.001）。在输注PE并叠加NP（仅激活ABR）期间，平均动脉压进一步升高至101.·2±2.9 mmHg（与对照组或单独输注PE相比，p<0.001），心率恢复到62.9±2.0次/分钟的对照水平（与对照组相比，p=无显著性差异；与PE组相比，PE加NP组p<0.01），但MSNA仍降至48.6±9.2单位（与对照组相比，p<0.01；与单独输注PE相比，p=无显著性差异）。因此，联合激活ABR和CBR导致MSNA降低65±5%，而仅激活ABR导致MSNA降低73±7%。在另一组针对7名受试者的实验（第二组）中，我们仅使用持续的颈部外部吸引来激活CBR（使ABR保持不变或最小程度失活），并研究了MSNA对这种CBR激活的反应。（摘要截断于400字）
