Smith S A, Querry R G, Fadel P J, Weiss M W, Olivencia-Yurvati A, Shi X, Raven P B
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth 76107, USA.
Auton Neurosci. 2001 Apr 12;88(1-2):74-85. doi: 10.1016/S1566-0702(01)00214-4.
In order to characterize the stimulus-response relationships of the arterial, aortic, and carotid baroreflexes in mediating cardiac chronotropic function, we measured heart rate (HR) responses elicited by acute changes in mean arterial pressure (MAP) and carotid sinus pressure (CSP) in 11 healthy individuals. Arterial (aortic + carotid) baroreflex control of HR was quantified using ramped changes in MAP induced by bolus injection of phenylephrine (PE) and sodium nitroprusside (SN). To assess aortic-cardiac responses, neck pressure (NP) and suction (NS) were applied during PE and SN administration, respectively, to counter alterations in CSP thereby isolating the aortic baroreflex. Graded levels of NP and NS were delivered to the carotid sinus using a customized neck collar device to assess the carotid-cardiac baroreflex, independent of drug infusion. The operating characteristics of each reflex were determined from the logistic function of the elicited HR response to the induced change in MAP. The arterial pressures at which the threshold was located on the stimulus-response curves determined for the arterial, aortic and carotid baroreflexes were not significantly different (72+/-4, 67+/-3, and 72+/-4 mm Hg, respectively, P > 0.05). Similarly, the MAP at which the saturation of the reflex responses were elicited did not differ among the baroreflex arcs examined (98+/-3, 99+/-2, and 102+/-3 mm Hg, respectively). These data suggest that the baroreceptor populations studied operate over the same range of arterial pressures. This finding indicates each baroreflex functions as both an important anti-hypotensive and anti-hypertensive mechanism. In addition, this investigation describes a model of aortic baroreflex function in normal healthy humans, which may prove useful in identifying the origin of baroreflex dysfunction in disease- and training-induced conditions.
为了描述动脉、主动脉和颈动脉压力反射在调节心脏变时功能中的刺激-反应关系,我们测量了11名健康个体中平均动脉压(MAP)和颈动脉窦压力(CSP)急性变化所引发的心率(HR)反应。通过静脉注射去氧肾上腺素(PE)和硝普钠(SN)诱导MAP的斜坡变化,对动脉(主动脉+颈动脉)压力反射对HR的控制进行量化。为了评估主动脉-心脏反应,在给予PE和SN期间分别施加颈部压力(NP)和吸引(NS),以抵消CSP的变化,从而分离主动脉压力反射。使用定制的颈圈装置向颈动脉窦施加不同水平的NP和NS,以评估颈动脉-心脏压力反射,而不受药物输注的影响。根据诱发的HR反应对诱导的MAP变化的逻辑函数来确定每个反射的操作特征。在为动脉、主动脉和颈动脉压力反射确定的刺激-反应曲线上,阈值所在的动脉压没有显著差异(分别为72±4、67±3和72±4 mmHg,P>0.05)。同样,在所检查的压力反射弧中,引发反射反应饱和时的MAP也没有差异(分别为98±3、99±2和102±3 mmHg)。这些数据表明,所研究的压力感受器群体在相同的动脉压范围内起作用。这一发现表明,每个压力反射既是一种重要的抗低血压机制,也是一种重要的抗高血压机制。此外,本研究描述了正常健康人类主动脉压力反射功能的模型,这可能有助于识别疾病和训练诱发情况下压力反射功能障碍的起源。