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1 Laboratoire de Physiologie Respiratoire, Faculté de Médecine, St.-Antoine, Université Pierre et Marie Curie, 75012 Paris, France; and 2 Institute of Pathological Physiology, Charles University, Prague, Czech Republic
We
investigated whether an hypoxia-induced increase in airway resistance
mediated by vagal efferents participates in the increase in
end-expiratory lung volume (EELV) observed in hypoxia. We also assessed
the contribution of the end-expiratory activity of the diaphragm
(DE) to this phenomenon.
Therefore, we measured EELV, total lung resistance
(RL), dynamic lung compliance
(Cdyn), DE, and minute
ventilation (
E) in anesthetized rats
during normoxia and hypoxia (10%
O2) before (control) and after
administration of atropine or saline. In the control group, hypoxia
increased EELV, Cdyn, DE, and
E but slightly decreased
RL. These changes were
unaffected by saline or atropine, except that, in the atropine-treated rats, hypoxia did not change RL.
These results suggest that 1) the
increase in EELV observed in hypoxia cannot result from an increase in
airway resistance; 2) the increased
and persistent activity of inspiratory muscles during expiration is the
most likely cause of the increase in EELV during hypoxia; and
3) the decrease in
RL induced by hypoxia could
result from the increase in lung volume including EELV.
total lung resistance; dynamic lung compliance; end-expiratory activity of the diaphragm; postinspiratory inspiratory activity; atropine; braking of expiratory airflow
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