Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans.

Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans.
复制标题

主动脉压力反射在低血压期间调节交感神经反应中的重要性。

DOI:
10.1161/01.cir.79.1.83
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发表时间:
1989
期刊:
影响因子:
37.8
通讯作者:
Ferguson,DW
Ferguson,DW
中科院分区:
医学1区
文献类型:
--
作者:
Sanders,JS;Mark,AL;Ferguson,DW

文献摘要

被引文献

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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期间反射性地调节心率和外周血管反应。这两个动脉压力反射通路对这些自主反应的控制的相对影响是有争议的。我们实验室最近的研究表明,主动脉压力反射产生实质性的和持续的抑制传出交感神经活动的肌肉(MSNA)在动脉压的增加。在低血压期间,这两种压力反射对人类MSNA的调节,特别是主动脉压力反射的作用,仍然不确定。因此,我们进行了一系列新的研究,以评估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± SEM)的正常男性受试者中,我们直接测量了静脉输注硝普钠和叠加应用颈外吸引的硝普钠输注期间产生的低血压(主动脉和颈动脉压力感受器失活)的平均动脉压、心率、中心静脉压和MSNA(显微神经造影术)。颈部抽吸的水平足以维持透壁颈动脉窦压力高于对照水平(颈动脉压力感受器激活),而主动脉压力反射保持失活。中心静脉压通过容量输注保持恒定。我们还研究了这些相同的主题直接颈动脉压力感受器失活与颈部外压力的应用程序的反应。在单独的颈部压力期间,平均动脉压有反射性增加;因此,在该方案的这一部分期间,我们实现了颈动脉压力感受器失活和一些主动脉压力感受器激活。硝普钠输液(联合主动脉和颈动脉失活)将平均动脉压从90.8 +/- 3.1降至77.8 +/- 1.1 mm Hg(p <0.01)伴随心率从62.6 +/- 3.0次/分增加至89.7 +/- 6.1次/分MSNA从273.8 +/- 43.0至950.6 +/- 133.5单位(p <0.001)。在持续硝普钠输注并叠加颈部吸引期间(主动脉压力感受器失活和颈动脉压力感受器激活),平均动脉压降至70.3 ± 1.9 mm Hg(与对照组相比,p <0.001),心率降至82.5 +/- 6.5次/min(p小于0.01,与对照组或单独使用硝普钠相比),但MSNA仍显著增加至889.7 +/- 105.1单位(p小于0.001,与对照组相比; p = NS与单独使用硝普钠相比)。(400字处截断摘要)
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)