This investigation was designed primarily to study three closely related questions about rhythmic breathing: a) how is apneusis (apneustic respiration) initiated and modified? b) Is the isolated medulla oblongata capable of producing rhythmic respiration? c) What mechanism generates the rhythm of normal breathing? The changes of respiratory pattern were studied in 131 mid-collicular decerebrate cats following serial transections of the brain stem at various levels, vagotomy and elimination of other peripheral receptors. a) It is concluded that a tonically active pontile center produces apneustic respiration, is anatomically and functionally distinct from the medullary inspiratory center, and is almost certainly not a part of the reticular facilitatory system. Afferent impulses from the carotid receptors may influence but do not initiate apneusis. b) The isolated medulla can maintain rhythmic respiration without the influence of spinal or vagal afferents but only under special conditions. However, the medullary respiratory centers are not the pacemakers for normal respiration. c) A new schema is proposed tentatively for the neural organization of normal respiratory rhythmicity. It is suggested that in normal respiration the rhythm originates in the pontile apneustic center with periodic modulation by inhibitory impulses from the pulmonary stretch receptors in the vagus and from the pneumotaxic center in the rostral pons.
It was shown previously by Chinn and Wang that dogs exposed to 800 r total body irradiation vomited within 2 hours after completion of exposure. After chronic destruction of the chemoceptive emetic trigger zone, no dogs vomited within 2 hours of radiation. It was observed that these operated animals would vomit later throughout their period of survival. Visceral deafferentation alone (abdominal vagotomy and sympathectomy) did not prevent dogs from vomiting soon after irradiation or within several days. On the other hand, both acute and delayed emesis due to irradiation was not observed in dogs with chronic destruction of the chemoceptive trigger zone and abdominal visceral deafferentation. It appeared, therefore, that delayed vomiting following lethal total body irradiation was mediated through two mechanisms; the centrally located trigger zone, and the peripheral visceral afferent receptors of the vagus and sympathetic trunks.
Motion sickness was experimentally induced in dogs by means of a standardized swinging exposure. Susceptible dogs were selected for surgical extirpation of the labyrinths or various parts of the cerebellum. It was found that animals showed no vomiting responses to long exposures of swinging motion after bilateral labyrinthectomy or ablation of the nodulus and uvula. Even with incomplete extirpation of these structures, animals would become partially or totally resistant to motion sickness. In general, these operated animals exhibited normal responses to intravenously administered apomorphine or orally administered copper sulfate. These results indicate that motion stimulates the labyrinthine receptors, and the vestibular impulses traverse the nodulus and uvula of the cerebellum, and the chemoceptive emetic trigger zone, and finally reach the medullary vomiting center.
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