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Animal experiment demonstrates brainstem and forebrain regulation of hypocapnic polypnea in cats, indicating distinct rostral neural networks modulate respiratory rate and amplitude.
The phrenic nerve discharge was recorded in locally anesthetized, vagotomized cats which were immobilized with gallamine. When the alveolar CO 2 tension is reduced, there is a decrease in phrenic discharge, as well as an increase of respiratory frequency, which may become as high as several cycles per second ("hypocapnic polypnea"). Diencephalic section (level of optic chiasma) results in a marked increase of phrenic discharge during hypocapnia; it is therefore concluded that forebrain structures may exert a tonic inhibitory effect on inspiratory discharge. While diencephalic section does not prevent hypocapnic polypnea, mesencephalic section (intercollicular level) eliminates the phenomenon or drastically reduces its extent; it is therefore concluded that at the posterior diencephalic and upper midbrain levels there are systems whose tonic activity tends to increase the respiratory frequency. In naturally breathing, midcollicular decerebrate cats, it was found that CO 2 inhalation while the vagi are intact causes an increase of respiratory frequency, whereas after vagotomy it causes a decrease of frequency; thus, vagal afferent input results in reversal of the phenomenon of hypocapnic polypnea.
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Morton I. Cohen (1964) studied this question.
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