Arterial pulse modulated activity is expressed in respiratory neural output.
Although it is well-established that sympathetic activity is modulated with respiration, it is unknown whether neural control of respiration is reciprocally influenced by cardiovascular function. Even though previous studies have suggested the existence of pulse modulation in respiratory neurons, they could not exclude the possibility that such cells were involved in cardiovascular rather than respiratory motor control, owing to neuroanatomic and functional overlaps between brain stem neurons involved in respiratory and cardiovascular control. The aim of this study was to test the hypothesis that respiratory motoneurons and putative premotoneurons are modulated by arterial pulse. An existing data set composed of 72 well-characterized, respiratory-modulated brain stem motoneurons and putative premotoneurons was analyzed using delta(2), a recently described statistic that quantifies the magnitude of arterial pulse-modulated spike activity [Dick TE and Morris KF. J Physiol 556: 959-970, 2004]. Neuronal activity was recorded in the rostral and caudal ventral respiratory groups of 19 decerebrate, neuromuscular-blocked, ventilated cats. Axonal projections were identified by rectified and unrectified spike-triggered averages of recurrent laryngeal nerve activity or by antidromic activation from spinal stimulation electrodes. The firing rates of approximately 30% of these neurons were modulated in phase with both the respiratory and cardiac cycles. Furthermore, arterial pulse modulation occurred preferentially in the expiratory phase in that only expiratory neurons had high delta(2) values and only expiratory activity had significant delta(2) values after partitioning tonic activity into the inspiratory and expiratory phases. The results demonstrate that both respiratory motoneurons and putative premotoneuronal activity can be pulse modulated. We conclude that a cardiac cycle-related modulation is expressed in respiratory motor activity, complementing the long-recognized respiratory modulation of sympathetic nerve activity.
Dick
Thomas E
TE
Division of Pulmonary and Critical Care Medicine, Dept. of Medicine, Case Western Reserve University, Biomedical Research Bldg. BRB B55, 10900 Euclid Avenue, Cleveland, OH 44106-4941, USA. thomas.dick@case.edu
Shannon
Roger
R
Lindsey
Bruce G
BG
Nuding
Sarah C
SC
Segers
Lauren S
LS
Baekey
David M
DM
Morris
Kendall F
KF
D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001683:Biological Clocks / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002415:Cats; D003655:Decerebrate State; D005246:Feedback / Q000502:physiology; D006339:Heart Rate / Q000502:physiology*; D008168:Lung / Q000294:innervation* / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology*; D012123:Pulmonary Ventilation / Q000502:physiology*