Excitation of phrenic and sympathetic output during acute hypoxia: contribution of medullary oxygen detectors.

Severe brain hypoxia results in respiratory excitation and an increase in sympathetic nerve activity. Respiratory excitation takes the form of gasping which is characterized by an abrupt onset, high amplitude, short duration burst of inspiratory activity. Recent evidence suggests that centrally-mediated hypoxic respiratory and sympathetic excitation may result from direct hypoxic stimulation of discrete hypoxia chemosensitive sites in the medulla. Thus, medullary regions involved in the generation and modulation of respiratory and sympathetic vasomotor output may contain neurons which function as central oxygen detectors, acting as medullary analogs to the peripheral (arterial) chemoreceptors. This review focuses on the medullary sites and mechanisms proposed to mediate hypoxic respiratory and sympathetic excitation in anesthetized, chemodeafferented animals, and provides the evidence suggesting a role for central oxygen detectors in the control of breathing and sympathetic vasomotor output.