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Lung mechanics and end-expiratory lung volume during hypoxia in rats
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| Zeitschriftentitel: | Journal of Applied Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | Journal of Applied Physiology, 87, 1999, 1, S. 15-21 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Bonora, M. Vizek, M. Bonora, M. Vizek, M. |
|---|---|
| author |
Bonora, M. Vizek, M. |
| spellingShingle |
Bonora, M. Vizek, M. Journal of Applied Physiology Lung mechanics and end-expiratory lung volume during hypoxia in rats Physiology (medical) Physiology |
| author_sort |
bonora, m. |
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Bonora, M. Vizek, M. 8750-7587 1522-1601 American Physiological Society Physiology (medical) Physiology http://dx.doi.org/10.1152/jappl.1999.87.1.15 <jats:p> 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% O<jats:sub>2</jats:sub>) 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. </jats:p> Lung mechanics and end-expiratory lung volume during hypoxia in rats Journal of Applied Physiology |
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| title |
Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_unstemmed |
Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_full |
Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_fullStr |
Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_full_unstemmed |
Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_short |
Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_sort |
lung mechanics and end-expiratory lung volume during hypoxia in rats |
| topic |
Physiology (medical) Physiology |
| url |
http://dx.doi.org/10.1152/jappl.1999.87.1.15 |
| publishDate |
1999 |
| physical |
15-21 |
| description |
<jats:p> 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% O<jats:sub>2</jats:sub>) 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. </jats:p> |
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| description | <jats:p> 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% O<jats:sub>2</jats:sub>) 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. </jats:p> |
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| spelling | Bonora, M. Vizek, M. 8750-7587 1522-1601 American Physiological Society Physiology (medical) Physiology http://dx.doi.org/10.1152/jappl.1999.87.1.15 <jats:p> 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% O<jats:sub>2</jats:sub>) 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. </jats:p> Lung mechanics and end-expiratory lung volume during hypoxia in rats Journal of Applied Physiology |
| spellingShingle | Bonora, M., Vizek, M., Journal of Applied Physiology, Lung mechanics and end-expiratory lung volume during hypoxia in rats, Physiology (medical), Physiology |
| title | Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_full | Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_fullStr | Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_full_unstemmed | Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_short | Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_sort | lung mechanics and end-expiratory lung volume during hypoxia in rats |
| title_unstemmed | Lung mechanics and end-expiratory lung volume during hypoxia in rats |
| topic | Physiology (medical), Physiology |
| url | http://dx.doi.org/10.1152/jappl.1999.87.1.15 |