Journal of Applied Physiology, Vol 56, Issue 6 1583-1588, Copyright © 1984 by American Physiological Society
Respiratory response to partial paralysis in anesthetized dogs
A. Oliven, E. C. Deal Jr, S. G. Kelsen and N. S. Cherniack
The ability to maintain alveolar ventilation is compromised by respiratory
muscle weakness. To examine the independent role of reflexly mediated
neural mechanisms to decreases in the strength of contraction of
respiratory muscles, we studied the effects of partial paralysis on the
level and pattern of phrenic motor activity in 22 anesthetized
spontaneously breathing dogs. Graded weakness induced with succinylcholine
decreased tidal volume and prolonged both inspiratory and expiratory time
causing hypoventilation and hypercapnia. Phrenic peak activity as well as
the rate of rise of the integrated phrenic neurogram increased. However,
when studied under isocapnic conditions, increases in the severity of
paralysis, as assessed from the ratio of peak diaphragm electromyogram to
peak phrenic activity, produced progressive increases in inspiratory time
and phrenic peak activity but did not affect its rate of rise. After
vagotomy, partial paralysis induced in 11 dogs with succinylcholine also
prolonged the inspiratory burst of phrenic activity, indicating that vagal
reflexes were not solely responsible for the alterations in respiratory
timing. Muscle paresis was also induced with gallamine or dantrolene,
causing similar responses of phrenic activity and respiratory timing. Thus,
at constant levels of arterial CO2 in anesthetized dogs, respiratory muscle
partial paralysis results in a decrease in breathing rate without changing
the rate of rise of respiratory motor activity. This is not dependent
solely on vagally mediated reflexes and occurs regardless of the
pharmacological agent used. These observations in the anesthetized state
are qualitatively different from the response to respiratory muscle
paralysis or weakness observed in awake subjects.(ABSTRACT TRUNCATED AT 250
WORDS)
