Faculty Opinions recommendation of BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia.

2004 ◽  
Author(s):  
Jack Feldman
Keyword(s):  
Intermittent Hypoxia ◽  
Respiratory Plasticity ◽  
Necessary And Sufficient

BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia

2003 ◽  
Vol 7 (1) ◽  
pp. 48-55 ◽  
Author(s):  
Tracy L Baker-Herman ◽  
David D Fuller ◽  
Ryan W Bavis ◽  
Andrea G Zabka ◽  
Francis J Golder ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Respiratory Plasticity ◽  
Necessary And Sufficient

scholarly journals Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation

2015 ◽  
Vol 46 (4) ◽  
pp. 1072-1083 ◽  
Author(s):  
Andrew E. Beaudin ◽  
Xavier Waltz ◽  
Matiram Pun ◽  
Katherine E. Wynne-Edwards ◽  
Sofia B. Ahmed ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Sleep Apnoea ◽  
Double Blind ◽  
Healthy Humans ◽  
Cox Inhibitor ◽  
Obstructive Sleep ◽  
Tnf Α ◽  
Respiratory Plasticity ◽  
Cox 2

Ventilatory instability, reflected by enhanced acute hypoxic (AHVR) and hypercapnic (AHCVR) ventilatory responses is a fundamental component of obstructive sleep apnoea (OSA) pathogenesis. Intermittent hypoxia-induced inflammation is postulated to promote AHVR enhancement in OSA, although the role of inflammation in intermittent hypoxia-induced respiratory changes in humans has not been examined. Thus, this study assessed the role of inflammation in intermittent hypoxia-induced respiratory plasticity in healthy humans.In a double-blind, placebo-controlled, randomised crossover study design, 12 males were exposed to 6 h of intermittent hypoxia on three occasions. Prior to intermittent hypoxia exposures, participants ingested (for 4  days) either placebo or the nonsteroidal anti-inflammatory drugs indomethacin (nonselective cyclooxygenase (COX) inhibitor) and celecoxib (selective COX-2 inhibitor). Pre- and post-intermittent hypoxia resting ventilation, AHVR, AHCVR and serum concentration of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α were assessed.Pre-intermittent hypoxia resting ventilation, AHVR, AHCVR and TNF-α concentrations were similar across all three conditions (p≥0.093). Intermittent hypoxia increased resting ventilation and the AHVR similarly across all conditions (p=0.827), while the AHCVR was increased (p=0.003) and TNF-α was decreased (p=0.006) with only selective COX-2 inhibition.These findings indicate that inflammation does not contribute to human intermittent hypoxia-induced respiratory plasticity. Moreover, selective COX-2 inhibition augmented the AHCVR following intermittent hypoxia exposure, suggesting that selective COX-2 inhibition could exacerbate OSA severity by increasing ventilatory instability.

scholarly journals Reactive oxygen species and respiratory plasticity following intermittent hypoxia

2008 ◽  
Vol 164 (1-2) ◽  
pp. 263-271 ◽  
Author(s):  
P.M. MacFarlane ◽  
J.E.R. Wilkerson ◽  
M.R. Lovett-Barr ◽  
G.S. Mitchell
Keyword(s):  
Reactive Oxygen Species ◽  
Intermittent Hypoxia ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Respiratory Plasticity

scholarly journals Unexpected Benefits of Intermittent Hypoxia: Enhanced Respiratory and Nonrespiratory Motor Function

Physiology ◽  
2014 ◽  
Vol 29 (1) ◽  
pp. 39-48 ◽  
Author(s):  
E. A. Dale ◽  
F. Ben Mabrouk ◽  
G. S. Mitchell
Keyword(s):  
Nervous System ◽  
Motor Function ◽  
Intermittent Hypoxia ◽  
Low Dose ◽  
Spinal Injury ◽  
Trophic Factors ◽  
Systemic Hypertension ◽  
Cellular Mechanisms ◽  
Clinical Disorders ◽  
Respiratory Plasticity

Intermittent hypoxia (IH) is most often thought of for its role in morbidity associated with sleep-disordered breathing, including central nervous system pathology. However, recent evidence suggests that the nervous system fights back in an attempt to minimize pathology by increasing the expression of growth/trophic factors that confer neuroprotection and neuroplasticity. For example, even modest (“low dose”) IH elicits respiratory motor plasticity, increasing the strength of respiratory contractions and breathing. These low IH doses upregulate hypoxia-sensitive growth/trophic factors within respiratory motoneurons but do not elicit detectable pathologies such as hippocampal cell death, neuroinflammation, or systemic hypertension. Recent advances have been made toward understanding cellular mechanisms giving rise to IH-induced respiratory plasticity, and attempts have been made to harness the benefits of low-dose IH to treat respiratory insufficiency after cervical spinal injury. Our recent realization that IH also upregulates growth/trophic factors in nonrespiratory motoneurons and improves limb (or leg) function after incomplete chronic spinal injuries suggests that IH-induced plasticity is a general feature of motor systems. Collectively, available evidence suggests that low-dose IH may represent a safe and effective treatment to restore lost motor function in diverse clinical disorders that impair motor function.

scholarly journals Spinal respiratory plasticity is impaired by two models of systemic inflammation, lipopolysaccharide and severe intermittent hypoxia

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Adrianne G Huxtable ◽  
Timothy Peterson ◽  
Stephanie M Smith ◽  
Jyoti J Watters ◽  
Gordon S Mitchell
Keyword(s):  
Systemic Inflammation ◽  
Intermittent Hypoxia ◽  
Respiratory Plasticity
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