Smith C A, Harms C A, Henderson K S, Dempsey J A
John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison 53705-2368, USA.
J Appl Physiol (1985). 1997 Mar;82(3):791-8. doi: 10.1152/jappl.1997.82.3.791.
Specific carotid body (CB) hypocapnia in the-10-Torr (less than eupneic) range reduced ventilation in the awake and sleeping dog to the same degree as did CB hyperoxia [CB PO2 (PCBO2); > 500 Torr; C.A. Smith, K.W. Saupe, K. S. Henderson, and J. A. Dempsey. J. Appl. Physiol. 79:689-699, 1995], suggesting a powerful inhibitory effect of hypocapnia at the carotid chemosensor over a range of PCO2 encountered commonly in physiological hyperpneas. The primary purpose of this study was to assess the ventilatory effect of CB hypocapnia on the ventilatory response to concomitant CB hypoxia. The secondary purpose was to assess the relative gains of the CB and central chemoreceptors to hypocapnia. In eight awake female dogs the vascularly isolated CB was perfused with hypoxic blood (mild, PCBO2 approximately equal to 50 Torr or severe, PCBO2 approximately equal to 36 Torr) in a background of normocapnia or hypocapnia (10 Torr less than eupneic arterial PCO2) in the perfusate. The systemic (and brain) circulation was normoxic throughout, and arterial PCO2 was not controlled (poikilocapnia). With CB hypocapnia, the peak ventilation (range 19-27 s) in response to hypoxic CB perfusion increased 48% (mild) and 77% (severe) due to increased tidal volume. When CB hypocapnia was present, these increases in ventilation were reduced to 21 and 27%, respectively. With systemic hypocapnia, with the isolated CB maintained normocapnic and hypoxic for > 70 s, the steady-state poikilocapnic ventilatory response (i.e., to systemic hypocapnia alone) decreased 15% (mild CB hypoxia) and 27% (severe CB hypoxia) from the peak response, respectively. We conclude that carotid body hypocapnia can be a major source of inhibitory feedback to respiratory motor output during the hyperventilatory response to hypoxic carotid body stimulation.
在清醒和睡眠的犬类中，颈动脉体（CB）低碳酸血症处于-10托（低于平静呼吸水平）范围时，其降低通气的程度与CB高氧血症[CB PO2（PCBO2）> 500托；C.A.史密斯、K.W.索普、K.S.亨德森和J.A.登普西。《应用生理学杂志》79:689 - 699，1995]相同，这表明在生理呼吸增强时常见的PCO2范围内，低碳酸血症对颈动脉化学感受器具有强大的抑制作用。本研究的主要目的是评估CB低碳酸血症对伴随CB低氧血症时通气反应的通气效应。次要目的是评估CB和中枢化学感受器对低碳酸血症的相对增益。在八只清醒的雌性犬中，在灌注液中常碳酸血症或低碳酸血症（动脉PCO2比平静呼吸时低10托）的背景下，用低氧血液（轻度，PCBO2约等于50托或重度，PCBO2约等于36托）灌注血管分离的CB。整个过程中全身（和脑部）循环为常氧状态，且未控制动脉PCO2（变碳酸血症）。在CB低碳酸血症情况下，由于潮气量增加，对低氧CB灌注的峰值通气（范围19 - 27秒）分别增加了48%（轻度）和77%（重度）。当存在CB低碳酸血症时，这些通气增加分别降至21%和27%。在全身低碳酸血症情况下，分离的CB维持常碳酸血症和低氧状态超过70秒，稳态变碳酸血症通气反应（即仅对全身低碳酸血症的反应）分别比峰值反应降低了15%（轻度CB低氧血症）和27%（重度CB低氧血症）。我们得出结论，在对低氧颈动脉体刺激的过度通气反应过程中，颈动脉体低碳酸血症可能是呼吸运动输出抑制性反馈的主要来源。
