Mancia G
Circ Res. 1975 Feb;36(2):270-6. doi: 10.1161/01.res.36.2.270.
The modification by the carotid baroreceptors of the vascular responses to chemoreceptor stimulation was studied in anesthetized, artificially ventilated, vagotomized dogs. The carotid bifurcations were vascularly isolated and perfused with blood at constant pressures of 134, 215, and 51 mm Hg to cause intermediate, maximal, and minimal inhibition, respectively, of the vasomotor center. At each pressure, stimulation of the carotid chemoreceptors was achieved by perfusion with hypoxic hypercapnic blood. With intermediate inhibition, the chemoreceptor stimulation increased the aortic pressure by 50% and decreased the hind-limb and kidney blood flow (perfusion at constant pressure) by 59% and 19%, respectively. At carotid sinus pressures of 215 and 51 mm Hg, the effects of chemoreceptor stimulation were absent or markedly attenuated. With intermediate sinus pressure, chemoreceptor stimulation decreased the perfusion pressure of the saphenous vein by 27% (perfusion at constant flow). When the sinus pressure was increased to 215 mm Hg, the tone of the vein did not change, but chemoreceptor stimulation was without effect. The present study indicates a central interaction (which may be presynaptic) between the chemoreceptor and baroreceptor inputs such that the vascular responses to chemoreceptor stimulation are inhibited when the carotid sinus activity is maximal or minimal.
在麻醉、人工通气、迷走神经切断的犬中，研究了颈动脉压力感受器对化学感受器刺激所引起的血管反应的调节作用。将颈动脉分叉处进行血管分离，并分别以134、215和51 mmHg的恒定压力灌注血液，以分别引起血管运动中枢的中度、最大程度和最小程度抑制。在每个压力水平下，通过灌注低氧高碳酸血症血液来刺激颈动脉化学感受器。在中度抑制时，化学感受器刺激使主动脉压升高50%，后肢和肾脏血流量（恒压灌注）分别减少59%和19%。在颈动脉窦压力为215和51 mmHg时，化学感受器刺激的效应消失或明显减弱。在中度窦压时，化学感受器刺激使隐静脉灌注压降低27%（恒流灌注）。当窦压升至215 mmHg时，静脉张力未改变，但化学感受器刺激无效。本研究表明化学感受器和压力感受器传入之间存在中枢相互作用（可能是突触前的），使得当颈动脉窦活动处于最大或最小时，对化学感受器刺激的血管反应受到抑制。
