Phrenic nerve responses to hypoxia and CO 2 in decerebrate dogs

Abstract

Phrenic responses to isocapnic hypoxia and hypercapnia were studied using paralyzed vagotomized dogs (either decerebrate or chloralose-anesthetized). The hypoxia-induced increase in phrenic minute activity (PMA) was significantly greater in anesthetized dogs when compared with the response observed in decerebrate dogs. Phrenic responses to hypercapnia were also significantly different in the two groups of dogs. Increases in phrenic amplitude (AMP) and frequency (FREQ) were observed in anesthetized dogs, whereas decerebrate dogs responded to CO 2 without a change in FREQ. Spontaneously breathing dogs (either decerebrate or anesthetized) were used for studying the effects of vagotomy on the integrated phrenic neurogram. Changes in phrenic pattern in response to vagotomy were qualitatively similar in anesthetized and decerebrate dogs. However, in decerebrate dogs, AMP was disproportionately increased relative to the decrease in FREQ such that PMA increased following vagal transection. Conversely, in anesthetized dogs, the increase in AMP and decrease in FREQ in response to vagotomy were proportional; PMA remained unchanged. These results suggest that mesencephalic decerebration disrupts neuronal circuits which participate in the chemical control of breathing. In addition, suprapontine structures may be involved in coupling FREQ and AMP (tidal volume) so that PMA (ventilation) is stabilized. Finally, these studies provide evidence for a vagally-independent frequency controller in dogs which is sensitive to hypoxia and hypercapnia, but appears to be highly dependent upon suprapontine structures.