Lung mechanics and end-expiratory lung volume during hypoxia in rats.
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 (VE) in anesthetized rats during normoxia and hypoxia (10% O(2)) before (control) and after administration of atropine or saline. In the control group, hypoxia increased EELV, Cdyn, DE, and VE 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.
Laboratoire de Physiologie Respiratoire, Faculté de Médecine, St. -Antoine, Université Pierre et Marie Curie, 75012 Paris, France.
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M
Bonora
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M
Vizek
D000403:Airway Resistance / Q000187:drug effects; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D003964:Diaphragm / Q000187:drug effects / Q000503:physiopathology; D004525:Efferent Pathways / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D008170:Lung Compliance / Q000187:drug effects; D008176:Lung Volume Measurements; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015656:Respiratory Mechanics / Q000187:drug effects; D014630:Vagus Nerve / Q000503:physiopathology
D001285:Atropine