Reversal of hypoxic bradycardia by halothane or midcollicular decerebration.
Previous work suggests a primary vagal bradycardia during hypoxic excitation of the arterial chemoreceptors. In this study we examined whether tachycardia, resulting from withdrawal of vagal inhibition of the cardiac pacemaker, may also occur during hypoxia. Cats with cervical spinal section were ventilated with hypoxic gas mixtures or allowed to remain apneic in expiration while heart rate was continually monitored. During recovery from halothane anesthesia or following electrolytic midcollicular decerebration, the bradycardic response to hypoxic or asphyxic stimulation was reduced or was reversed to tachycardia. The extent of reduction or reversal of the bradycardia was positively correlated with the level of the arterial pressure which was adjusted by either hemorrhage or infusion of phenylephrine. These findings indicate a tachycardic component of the vagal response to hypoxia, integrated in the pontomedullary region of the brainstem and resulting from interaction between the chemoreceptor and baroreceptor reflexes.
D000818:Animals; D001794:Blood Pressure; D001919:Bradycardia / Q000503:physiopathology; D001933:Brain Stem / Q000503:physiopathology; D002415:Cats; D002628:Chemoreceptor Cells / Q000503:physiopathology; D003655:Decerebrate State; D006221:Halothane / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D013268:Stimulation, Chemical; D014630:Vagus Nerve / Q000503:physiopathology*
D006221:Halothane