Prolonged Inhibition of Respiration Following Acute Hypoxia in Glomectomized Cats

Respiratory responses to several minutes exposure to hypoxia (PaO2 less than 30 torr) were determined in anesthetized, paralyzed, vagotomized and glomectomized cats whose end-tidal PCO2 and body temperature were kept constant. Respiratory activity was quantified from phrenic nerve activity. Animals breathed 100% O2 during the control period. The study reaffirmed that in glomectomized animals hypoxia causes depression of respiratory activity. The new finding was that phrenic activity remained significantly depressed below the original control level for more than one hr after return to the hyperoxic state. Medullary ECF pH was measured in 3 cats. There was an acid shift of pH during hypoxia that persisted for more than one hour after return to hyperoxic state. We pretreated another group (n = 5) of animals with theophylline, a specific antagonist of the inhibitory neurotransmitter adenosine. Hypoxia still caused depression of respiratory activity, but it was less severe than in untreated animals. Upon return to the hyperoxic state, respiratory activity returned to the original control level within 10 min. We conclude that the long-lasting depression of respiration following hypoxia is mediated by adenosine. Furthermore, adenosine appears to be partially responsible for the acute depression of respiration during the hypoxic exposure.