Fregosi R F, Hwang J C, Bartlett D, St John W M
Department of Physiology, Dartmouth Medical School, Hanover, NH.
Respir Physiol. 1992 Aug;89(2):179-94. doi: 10.1016/0034-5687(92)90049-3.
Our purpose was to examine the influence of hypercapnia on the activity of motoneurons innervating the transversus abdominis and internal oblique abdominal muscles, and of integrated phrenic and abdominal motor nerve activities. Studies were done in nine adult cats that were decerebrated, vagotomized, thoracotomized, paralyzed and ventilated mechanically. Of 42 motoneurons examined, 24 showed strong respiratory modulation (RM neurons), with the discharge confined primarily to the central expiratory period. The remaining 18 motoneurons discharged tonically, and failed to show respiratory modulation even at increased levels of central respiratory drive. Hyperoxic hypercapnia augmented the activities of the phrenic and abdominal nerves and increased the early expiratory discharge frequency of the RM neurons. The hypercapnia-induced increase in firing frequency during early expiration was accompanied by a corresponding decline in late expiration, and a virtual abolition of the inspiratory activity in the few neurons that discharged in this phase under normocapnic conditions. Finally, hypercapnia induced an increase in the number of spikes generated during each expiratory period in about half of the RM neurons, whereas the remaining cells showed a decrease. Thus, the increased peak activity of the integrated whole abdominal nerve burst with hypercapnia was brought about by a shift in the temporal pattern of motoneuron firing, or by an increase in the number of spikes generated during the expiratory period. The steep rate of rise and the pronounced early expiratory peak observed in the integrated abdominal nerve burst during hypercapnia in this preparation are consistent with the increase in motoneuron firing frequency during the early stages of the expiratory phase.
我们的目的是研究高碳酸血症对支配腹横肌和腹内斜肌的运动神经元活动以及膈神经和腹部运动神经综合活动的影响。研究在9只成年猫身上进行,这些猫被去大脑、切断迷走神经、开胸、麻痹并进行机械通气。在检查的42个运动神经元中,24个表现出强烈的呼吸调制(RM神经元),放电主要局限于呼气中期。其余18个运动神经元呈紧张性放电,即使在中枢呼吸驱动水平增加时也未表现出呼吸调制。高氧性高碳酸血症增强了膈神经和腹部神经的活动,并增加了RM神经元的早期呼气放电频率。高碳酸血症引起的早期呼气时放电频率增加伴随着晚期呼气时相应的下降,以及在正常碳酸血症条件下在此阶段放电的少数神经元的吸气活动几乎完全消失。最后,高碳酸血症使约一半的RM神经元在每个呼气期产生的峰电位数量增加,而其余细胞则减少。因此,高碳酸血症时腹部神经综合爆发的峰值活动增加是由运动神经元放电的时间模式改变或呼气期产生的峰电位数量增加引起的。在此准备过程中,高碳酸血症时腹部神经综合爆发中观察到的陡峭上升速率和明显的早期呼气峰值与呼气期早期运动神经元放电频率的增加一致。