Sanders J S, Mark A L, Ferguson D W
Department of Internal Medicine, University of Iowa Hospitals, Iowa City, 52242.
Circulation. 1989 Jan;79(1):83-92. doi: 10.1161/01.cir.79.1.83.
Arterial baroreceptors in the carotid sinus and aortic arch regions reflexly regulate heart rate and peripheral vascular responses during changes in arterial pressure. The relative influence of these two arterial baroreflex pathways on the control of these autonomic responses is debatable. Recent studies in our laboratory demonstrate that the aortic baroreflex produces substantial and sustained inhibition of efferent sympathetic nerve activity to muscle (MSNA) during increases in arterial pressure. The regulation of MSNA by these two baroreflexes in humans during hypotension, and particularly the role of the aortic baroreflex, remains undefined. We therefore performed a new series of studies to assess the relative influence of the aortic and carotid baroreflexes on MSNA responses during sustained decreases in arterial pressure. In eight normal male subjects, aged 23 +/- 1 years (mean +/- SEM), we directly measured mean arterial pressure, heart rate, central venous pressure, and MSNA (microneurography) during hypotension (combined aortic and carotid baroreceptor deactivation) produced by intravenous infusion of sodium nitroprusside and during nitroprusside infusion with superimposed application of external neck suction. Neck suction was applied at levels sufficient to maintain transmural carotid sinus pressure above control levels (carotid baroreceptor activation) while the aortic baroreflexes remained deactivated. Central venous pressure was maintained constant with volume infusion. We also studied responses of these same subjects to direct carotid baroreceptor deactivation with the application of external neck pressure. During neck pressure alone, there was a reflex increase in mean arterial pressure; thus, during this portion of the protocol, we achieved carotid baroreceptor deactivation with some aortic baroreceptor activation. Nitroprusside infusion (combined aortic and carotid deactivation) decreased mean arterial pressure from 90.8 +/- 3.1 to 77.8 +/- 1.1 mm Hg (p less than 0.01) with concomitant increases in heart rate from 62.6 +/- 3.0 to 89.7 +/- 6.1 beats/min (p less than 0.001) and in MSNA from 273.8 +/- 43.0 to 950.6 +/- 133.5 units (p less than 0.001). During continued nitroprusside infusion with superimposed neck suction (aortic baroreceptor deactivation and carotid baroreceptor activation), mean arterial pressure decreased to 70.3 +/- 1.9 mm Hg (p less than 0.001 vs. control), heart rate decreased to 82.5 +/- 6.5 beats/min (p less than 0.01 vs. control or vs. nitroprusside alone), but MSNA remained markedly increased at 889.7 +/- 105.1 units (p less than 0.001 vs. control; p = NS vs. nitroprusside alone).(ABSTRACT TRUNCATED AT 400 WORDS)
颈动脉窦和主动脉弓区域的动脉压力感受器在动脉压变化时可反射性调节心率和外周血管反应。这两条动脉压力感受性反射通路对这些自主反应控制的相对影响存在争议。我们实验室最近的研究表明，在动脉压升高时，主动脉压力感受性反射对肌肉传出交感神经活动（MSNA）产生显著且持续的抑制作用。在人类低血压期间，这两种压力感受性反射对MSNA的调节，尤其是主动脉压力感受性反射的作用，仍不明确。因此，我们进行了一系列新的研究，以评估在动脉压持续下降期间，主动脉和颈动脉压力感受性反射对MSNA反应的相对影响。在8名年龄为23±1岁（平均值±标准误）的正常男性受试者中，我们在静脉输注硝普钠导致的低血压（主动脉和颈动脉压力感受器联合失活）期间，以及在硝普钠输注并叠加颈部外部吸引时，直接测量平均动脉压、心率、中心静脉压和MSNA（微神经ography）。颈部吸引的施加水平足以使颈动脉窦跨壁压力维持在高于对照水平（颈动脉压力感受器激活），而主动脉压力感受性反射仍处于失活状态。通过容量输注使中心静脉压保持恒定。我们还研究了这些相同受试者对施加颈部外部压力导致的直接颈动脉压力感受器失活的反应。仅在颈部施加压力期间，平均动脉压有反射性升高；因此，在方案的这一部分期间，我们在一些主动脉压力感受器激活的情况下实现了颈动脉压力感受器失活。硝普钠输注（主动脉和颈动脉联合失活）使平均动脉压从90.8±3.1降至77.8±1.1 mmHg（p<0.01），同时心率从62.6±3.0增加至89.7±6.1次/分钟（p<0.001），MSNA从273.8±43.0增加至950.6±133.5单位（p<0.001）。在持续输注硝普钠并叠加颈部吸引（主动脉压力感受器失活和颈动脉压力感受器激活）期间，平均动脉压降至70.3±1.9 mmHg（与对照相比p<0.001），心率降至82.5±6.5次/分钟（与对照或单独使用硝普钠相比p<0.01），但MSNA仍显著升高至889.7±105.1单位（与对照相比p<0.001；与单独使用硝普钠相比p=无显著差异）。（摘要截断于400字）
