Lawson E E
J Appl Physiol Respir Environ Exerc Physiol. 1982 Jul;53(1):105-9. doi: 10.1152/jappl.1982.53.1.105.
The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (PCO2). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal PCO2. After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal PCO2 following long (30 s) stimuli, was independent of the end-tidal PCO2 level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.
本研究旨在探讨刺激持续时间和化学感觉输入对上喉神经（SLN）电刺激诱导的呼吸暂停后中枢呼吸活动恢复的影响。对小于8日龄的新生仔猪进行麻醉、麻痹，并在不同的呼气末二氧化碳分压（PCO2）水平下进行机械通气。在颈部双侧切断迷走神经。膈神经活动积分用作呼吸活动的指标。SLN刺激导致呼吸暂停，刺激停止后仍持续存在。刺激停止后呼吸暂停的时长与刺激持续时间直接相关，与呼气末PCO2呈负相关。呼吸暂停后，呼吸活动逐渐恢复到初始对照水平。使用时间的自然对数作为自变量的线性回归函数能很好地描述恢复模式。延长刺激持续时间会逐渐抑制呼吸暂停后初始呼吸活动的量。另一方面，呼吸恢复速率与刺激持续时间无关，并且除了在长时间（30秒）刺激后的低呼气末PCO2水平外，与呼气末PCO2水平无关。这些结果表明，一种长效的中枢机制调节由SLN刺激诱导的呼吸暂停后的恢复。
