Leitch A G, McLennan J E, Balkenhol S, McLaurin R L, Loudon R G
J Appl Physiol Respir Environ Exerc Physiol. 1980 Jul;49(1):52-8. doi: 10.1152/jappl.1980.49.1.52.
We have measured breath-by-breath instantaneous minute ventilation (VIinst) before, during, and after the administration of 10 breaths of 100% oxygen to seven male patients with head injury hyperventilation. The patients were hypoxemic (PaO2 61.2 +/- 6.3) and hypocapnic (PaCO2 26.6 +/- 5.9) with a respiratory alkalosis (pH 7.53 +/- 0.06) while breathing air. Following the oxygen VIinst fell on the average by 40 +/- 12.7% from 16.06 +/- 3.75 1.min-1 to a minimum of 9.73 +/- 3.20 1.min-1 at 20.4 +/- 2.9 s after the first breath of oxygen. In the majority of our hyperventilating patients, almost all of the resting hyperventilation could be abolished transiently by 100% oxygen. This fall in ventilation represents the peripheral chemoreceptor contribution to resting ventilation and is increased in the head injury patients in comparison with normal subjects breathing air or hypoxic gas mixtures, altitude-acclimatized subjects and patients who are hypoxic because of chronic bronchitis or interstitial lung disease. We suggest that the increased reflex hypoxic drive to ventilation found in our patients is secondary to their cerebral injury, resulting in a reduction of descending cortical inhibitory influences on the medullary respiratory control centers.
我们对7例头部受伤后进行过度通气的男性患者，在给予10次100%氧气呼吸之前、期间和之后，逐次测量了瞬时每分通气量（VIinst）。这些患者在呼吸空气时存在低氧血症（动脉血氧分压[PaO2]为61.2±6.3）、低碳酸血症（动脉血二氧化碳分压[PaCO2]为26.6±5.9）以及呼吸性碱中毒（pH值为7.53±0.06）。给予氧气后，VIinst平均下降了40±12.7%，从16.06±3.75升/分钟降至最低的9.73±3.20升/分钟，出现在首次呼吸氧气后20.4±2.9秒时。在我们大多数进行过度通气的患者中，几乎所有的静息过度通气都可被100%氧气短暂消除。这种通气量的下降代表了外周化学感受器对静息通气的贡献，并且与呼吸空气或低氧气体混合物的正常受试者、高原习服者以及因慢性支气管炎或间质性肺疾病导致低氧的患者相比，头部受伤患者的这一贡献有所增加。我们认为，在我们的患者中发现的对通气的反射性低氧驱动增加是继发于他们的脑损伤，导致大脑皮质对延髓呼吸控制中枢的下行抑制影响减弱。
