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Vol. 84, Issue 3, 922-932, March 1998
1 Department of Physiology, School of Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas 79430; and 2 Department of Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705
Mechanical ventilation of cats in sleep and wakefulness causes apnea, often within two to three cycles of the ventilator. We recorded 137 medullary respiratory neurons in four adult cats during eupnea and during apnea caused by mechanical ventilation. We hypothesized that the residual activity of respiratory neurons during apnea might reveal its cause(s). The results showed that residual activity depended on 1) the amount of nonrespiratory inputs to the cell (cells with more nonrespiratory inputs had greater amounts of residual activity); 2) the cell type (expiratory cells had more residual activity than inspiratory cells); and 3) the state of consciousness (more residual activity in wakefulness and rapid-eye-movement sleep than in non-rapid-eye-movement sleep). None of the cells showed an activation during ventilation that could explain the apnea. Residual activity of approximately one-half of the cells was modulated in phase with the ventilator. The strength of this modulation was quantified by using an effect-size statistic and was found to be weak. The patterns of modulation did not support the idea that mechanoreceptors excite some respiratory cells that, in turn, inhibit others. Indeed, most cells, inspiratory and expiratory, discharged during the deflation-inflation transition of ventilation. Residual activity failed to reveal the cause of apnea but showed that during apnea respiratory neurons act as if they were disinhibited and disfacilitated.
brain stem; respiratory network; cat; hypocapnea; mechanical ventilation
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