Abstract |
We hypothesized that reduced respiratory neural activity elicits compensatory mechanisms of plasticity that enhance respiratory motor output. In urethane-anesthetized and ventilated rats, we reversibly reduced respiratory neural activity for 25-30 min using: hypocapnia (end tidal CO(2)=30 mmHg), isoflurane (~1%) or high frequency ventilation (HFV; ~100 breaths/min). In all cases, increased phrenic burst amplitude was observed following restoration of respiratory neural activity ( hypocapnia: 92±22%; isoflurane: 65±22%; HFV: 54±13% baseline), which was significantly greater than time controls receiving the same surgery, but no interruptions in respiratory neural activity (3±5% baseline, p<0.05). Hypocapnia also elicited transient increases in respiratory burst frequency (9±2 versus 1±1bursts/min, p<0.05). Our results suggest that reduced respiratory neural activity elicits a unique form of plasticity in respiratory motor control which we refer to as inactivity-induced phrenic motor facilitation (iPMF). iPMF may prevent catastrophic decreases in respiratory motor output during ventilatory control disorders associated with abnormal respiratory activity.
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Authors | Safraaz Mahamed, Kristi A Strey, Gordon S Mitchell, Tracy L Baker-Herman |
Journal | Respiratory physiology & neurobiology
(Respir Physiol Neurobiol)
Vol. 175
Issue 3
Pg. 303-9
(Mar 15 2011)
ISSN: 1878-1519 [Electronic] Netherlands |
PMID | 21167322
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2011 Elsevier B.V. All rights reserved. |
Topics |
- Animals
- Hypocapnia
(physiopathology)
- Male
- Phrenic Nerve
(physiology)
- Rats
- Rats, Sprague-Dawley
- Respiratory Physiological Phenomena
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