Studinger Péter, Goldstein Richard, Taylor J Andrew
Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA 02114, USA.
J Physiol. 2007 Sep 15;583(Pt 3):1041-8. doi: 10.1113/jphysiol.2007.139204. Epub 2007 Jul 19.
According to conventional wisdom, hysteresis in cardiac vagal baroreflex function exhibits a specific pattern: pressure falls are associated with longer heart periods and a smaller linear gain. A similar pattern occurs in the pressure-diameter relationship of barosensory vessels, and therefore it has been suggested that baroreflex hysteresis derives solely from vascular behaviour. However, we hypothesized that mechanical and neural baroreflex components contribute equally to baroreflex hysteresis. Blood pressure, carotid diameter and the electrocardiogram were recorded continuously during two trials of sequential bolus injections of nitroprusside and phenylephrine in 14 young healthy subjects. Baroreflex gain and its mechanical and neural components were estimated for falls and rises in pressure and diameter. The position or set point of the relations was quantified at the mean pressure and mean diameter. Gains were determined via piecewise linear regression. Set points and gains for falls versus rises in pressure and diameter were compared with the Chow test. Hysteresis was observed in all individuals, but not in every trial. In most, but not all, trials pressure falls were associated with longer heart periods and smaller linear gain, as conventional wisdom would predict. However, the pattern of hysteresis derived from the interaction of both mechanical and neural components. The two components most often acted in opposition to determine differences in set point, but in conjunction to determine differences in baroreflex gain. Therefore, we conclude that hysteresis is not solely determined by barosensory vessel behaviour but by the complex interaction of mechanical and neural aspects of the arterial baroreflex.
按照传统观点，心脏迷走压力反射功能中的滞后现象呈现出一种特定模式：压力下降与更长的心搏间期以及更小的线性增益相关。在压力感受性血管的压力-直径关系中也会出现类似模式，因此有人提出压力反射滞后现象完全源于血管行为。然而，我们推测机械性和神经性压力反射成分对压力反射滞后现象的贡献是同等的。在14名年轻健康受试者中，在连续两次推注硝普钠和去氧肾上腺素的试验过程中，持续记录血压、颈动脉直径和心电图。针对压力和直径的下降及上升，估计压力反射增益及其机械性和神经性成分。在平均压力和平均直径处对关系的位置或设定点进行量化。通过分段线性回归确定增益。使用Chow检验比较压力和直径下降与上升时的设定点和增益。在所有个体中均观察到滞后现象，但并非在每个试验中都出现。在大多数（但并非全部）试验中，如传统观点所预测的那样，压力下降与更长的心搏间期和更小的线性增益相关。然而，滞后现象的模式源自机械性和神经性成分的相互作用。这两个成分最常以相反的方式作用以确定设定点的差异，但共同作用以确定压力反射增益的差异。因此，我们得出结论，滞后现象并非仅由压力感受性血管行为决定，而是由动脉压力反射的机械性和神经性方面的复杂相互作用所决定。
