J. E. Melton, S. C. Kadia, Q. P. Yu, J. A. Neubauer and N. H. Edelman Department of Medicine, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick 08903-0019, USA. In peripherally chemodenervated, vagotomized, chloralose-anesthetized cats, hypoxia can produce central cardiorespiratory depression or excitation depending on severity. We monitored phrenic and cervical sympathetic neurograms during either hypoxic depression or gasping and 30 min of subsequent isocapnic reoxygenation to determine whether the response of these outputs during hypoxia predicts their activity during recovery. Three levels of hypoxic response were produced in cats: 1) reduction of phrenic neurogram amplitude (PNA) by 30% fractional inspired O2 (FIO2) = 14-18%); 2) production of phrenic apnea (FIO2 = 9-10%); and 3) hypoxic gasping (FIO2 = 6-8%). Recovery from the milder levels of hypoxia was characterized by transient (< 10 min) depression of PNA and inspiratory synchronous sympathetic activity. Respiratory frequency was unaffected or only transiently depressed. Tonic sympathetic activity was unaffected. During reoxygenation after gasping, both PNA and inspiratory synchronous sympathetic activity were initially increased by 80% over control levels and respiratory frequency was depressed. Tonic sympathetic activity increased during hypoxia but returned to control levels after a brief undershoot on reoxygenation. All variables returned to control levels within 15 min. Measurement of medullary extracellular K+ concentration (K+e) in a separate group of cats indicated that a significant increase in this variable was associated with hypoxic gasping but was not correlated with PNA augmentation during reoxygenation. We hypothesize that increased K+e coincident with gasping may trigger a postanoxic potentiation of respiratory premotor neurons similar to that described in hippocampus.