Remmers J E, Marttila I
Respir Physiol. 1975 Jun;24(1):31-41. doi: 10.1016/0034-5687(75)90119-x.
Experiments designed to reveal an action of intercostal afferent stimulation on the rhythm of breathing were carried out on barbiturate-anesthetized, paralyzed cats, ventilated by a positive pressure respirator. Tetanic stimuli were applied to midthoracic, external intercostal nerves of intact animals and of animals displaying an apneustic pattern consequent to vagotomy and pontine lesions. In intact animals, the respiratory rhythm, as indicated by phrenic efferent activity, could be paced by intercostal nerve stimuli when they were timed to occur in a particular relationship to the lung volume cycle. Apparently, the action of the stimuli supplemented the phasic, volume-related afferent input. The response required considerable spatial summation and resulted from the action of intercostal afferents to either shorten inspiration or prolong expiration. These reflex effects could be attributed to activation of group II afferents. Although the actions of these afferents were relatively weak in the intact preparation, they proved potent in terminating an apneustic breath; brief stimuli, if they activated group II afferents, cut short phrenic discharge and initiated an expiratory phase, thereby restoring a reasonably normal respiratory rhythm.
在巴比妥类麻醉、麻痹的猫身上进行了旨在揭示肋间传入神经刺激对呼吸节律作用的实验,这些猫由正压呼吸器进行通气。对完整动物以及因迷走神经切断和脑桥损伤而呈现长吸式呼吸模式的动物的胸中段肋间神经施加强直刺激。在完整动物中,当肋间神经刺激与肺容积周期以特定关系定时发生时,膈传出活动所指示的呼吸节律可由肋间神经刺激来调节。显然,刺激的作用补充了与容积相关的阶段性传入输入。该反应需要相当程度的空间总和,是肋间传入神经缩短吸气或延长呼气作用的结果。这些反射效应可归因于Ⅱ类传入神经的激活。尽管这些传入神经在完整标本中的作用相对较弱,但它们在终止长吸式呼吸方面被证明是有效的;短暂刺激如果激活了Ⅱ类传入神经,会缩短膈放电并启动呼气阶段,从而恢复相当正常的呼吸节律。