Affiliation:
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
Abstract
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 (V˙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, andV˙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.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
16 articles.
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