Differential activation within costal diaphragm during rapid-eye-movement sleep in cats

Simultaneous recordings of the diaphragmatic electromyogram (EMG) were made from two separate regions of the costal diaphragm in six normal cats. The diaphragmatic activities were always synchronous and the amplitudes and rates of rise were similar during slow-wave sleep. In contrast, during natural rapid-eye-movement (REM) sleep, different activity was often present in the two leads. These differences were in the time of onset and offset, as well as in the amplitude and spike patterns, and occurred in approximately 5-20% of the diaphragmatic bursts averaged over the entire REM sleep period. With respect to eye movement density, the rate of differential activation was higher during periods of high density (26%) than in the absence of eye movements (1%) in the four animals for which these data were available. Differential activation of portions of the costal diaphragm is apparently a normal event of REM sleep. This could result from descending state-specific phasic neuronal activity that bypasses the medullary respiratory generator. Differential activation of portions of the diaphragm could contribute to disordered ventilation during REM sleep.

Central respiratory modulation of medullary sympathoexcitatory neurons in rat

The central respiratory generator exerts a modulatory influence on sympathetic nerve discharge. In cats the sympathoexcitatory neurons of the rostroventrolateral medulla (RVL) exhibit central respiratory modulation as well. Because RVL sympathoexcitatory neurons are largely responsible for the maintenance of sympathetic vasomotor tone, it is likely that the modulation of these neurons accounts for the central respiratory modulation of sympathetic discharge. In the present study experiments were performed to characterize the pattern of respiratory modulation of lumbar sympathetic nerve discharge (LSND) in the halothane-anesthetized rat. Phrenic-triggered averaging of LSND exhibited a small depression coincident with the onset of the phrenic burst followed by a large peak that was coincident with the cessation of the phrenic burst. Phrenic-triggered histograms of the activity of RVL sympathoexcitatory neurons exhibited three patterns of central respiratory modulation: inspiratory depression (I), inspiratory peak (II), and early inspiratory depression followed by a postinspiratory peak (III), a pattern that was very similar to that seen in LSND. Both nerve recording and single-unit recording experiments were performed in vagotomized rats with or without intact barosensory afferents. A comparison of the results suggested that, in the rat, the baroreflex does not modify or contribute to the central respiratory modulation of sympathetic output. Finally, a comparison was made between presumed nonadrenergic pacemaker-like neurons and putative C1 adrenergic neurons in the RVL. No differences were found in the patterns of central respiratory modulation.

Influence of phasic afferent information on phrenic neural output during hypercapnia

We measured the moving time average (MTA) of the phrenic neurogram before and after removal of phasic afferent information from the lungs, chest wall, and oscillations in blood gases by using constant-flow ventilation (CFV). Anesthetized dogs were studied at various levels of steady-state and progressive hypercapnia during spontaneous breathing and during CFV. When steady-state and progressive hypercapnia were compared, the frequency and height of the MTA phrenic neurogram were independent of the rate of induction of hypercapnia during each mode of ventilation. During spontaneous ventilation, the response to hypercapnia comprised mainly an increase in frequency with only a slight increase in the amplitude of the MTA phrenic waveform. During muscular paralysis and CFV, the responses were similar to those observed after vagotomy with mainly an increase in the amplitude and only a small increase in frequency. For both spontaneous breathing and CFV, increases in frequency were achieved mainly by a shortening in expiratory time with the inspiratory time remaining relatively constant. Our data support the concept of a centrally patterned respiratory generator, whose inherent pattern is modified by phasic feedback from peripheral receptors mainly of vagal origin.