Daly M D, Ward J, Wood L M
J Physiol. 1986 Sep;378:13-30. doi: 10.1113/jphysiol.1986.sp016205.
The reflex effects of increasing pulmonary ventilation on the responses of the hind-limb and systemic vascular resistances to stimulation of the carotid body chemoreceptors and carotid sinus baroreceptors and to distension of the urinary bladder have been studied in the anaesthetized dog. A preparation was used incorporating total cardiopulmonary bypass to maintain the arterial blood gas composition constant when alterations in pulmonary ventilation were made. The regions of both carotid bifurcations, the arch of the aorta and the cerebral circulation were independently perfused at constant pressure so as to exclude secondary reflexes from arterial baroreceptors. Four levels of pulmonary ventilation were used: 0.095, 0.285, 0.475 and 0.665 l min-1 kg-1 body weight, at a constant frequency of 19 cycles min-1. Increasing the pulmonary ventilation per se in steps from 0.095 to 0.665 l min-1 kg-1 resulted in a significant progressive reduction in hind-limb and systemic vascular resistances which were shown to be due to a reflex from the lungs. Stimulation of the carotid body chemoreceptors by hypoxic hypercapnic blood resulted in an increase in hind-limb and systemic vascular resistances when carried out at each of the four levels of pulmonary ventilation. The size of the increases in vascular resistances, however, was progressively and significantly reduced as the pulmonary ventilation was increased. This partial inhibition of the carotid body reflex vasoconstrictor response was dependent on the innervation of the lungs. Stimulation or unloading of the carotid sinus baroreceptors by altering the perfusion pressure in the vascularly isolated carotid bifurcation regions caused a significant decrease and increase respectively in hind-limb and systemic vascular resistances at all four levels of pulmonary ventilation. Unlike the responses to chemoreceptor stimulation, the size of these responses was unaffected by the level of pulmonary ventilation. Distension of the urinary bladder resulted in a significant increase in hind-limb and systemic vascular resistances. The size of these responses was also unaltered by changing the level of pulmonary ventilation. These results indicate that there is an interaction between the inputs from the lungs and the carotid body chemoreceptors in the control of hind-limb and systemic vascular resistances. In contrast the inputs from the carotid sinus baroreceptors and the urinary bladder were unaffected by the input from the lungs.
在麻醉犬身上研究了增加肺通气对后肢及全身血管阻力的反射效应,这些效应涉及刺激颈动脉体化学感受器、颈动脉窦压力感受器以及膀胱扩张时的反应。采用了一种包含全心肺转流的制备方法,以便在改变肺通气时维持动脉血气成分恒定。双侧颈动脉分叉区域、主动脉弓和脑循环区域均在恒定压力下独立灌注,以排除动脉压力感受器的继发反射影响。使用了四个肺通气水平:0.095、0.285、0.475和0.665升·分钟⁻¹·千克⁻¹体重,频率恒定为每分钟19次呼吸周期。肺通气量从0.095逐步增加到0.665升·分钟⁻¹·千克⁻¹本身会导致后肢和全身血管阻力显著逐渐降低,这表明是肺部反射所致。在四个肺通气水平的每一个水平上,用低氧高碳酸血症血液刺激颈动脉体化学感受器都会导致后肢和全身血管阻力增加。然而随着肺通气量增加,血管阻力增加的幅度会逐渐且显著降低。这种对颈动脉体反射性血管收缩反应的部分抑制取决于肺部的神经支配情况。通过改变血管隔离的颈动脉分叉区域的灌注压力来刺激或解除颈动脉窦压力感受器的负荷,在所有四个肺通气水平上,后肢和全身血管阻力分别显著降低和增加。与对化学感受器刺激的反应不同,这些反应的幅度不受肺通气水平的影响。膀胱扩张会导致后肢和全身血管阻力显著增加。改变肺通气水平也不会改变这些反应幅度。这些结果表明,在控制后肢和全身血管阻力方面,肺部输入与颈动脉体化学感受器输入之间存在相互作用;相比之下颈动脉窦压力感受器和膀胱传来的输入不受肺部输入影响