NDLI: Xanthine oxidase contributes to mechanical ventilation-induced diaphragmatic oxidative stress and contractile dysfunction.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Whidden, Melissa A. McClung, Joseph M. Falk, Darin J. Hudson, Matthew B. Smuder, Ashley J. Nelson, W. Bradley Powers, Scott K.
Description	Country affiliation: United States Author Affiliation: Whidden MA ( Dept. of Applied Physiology and Kinesiology, Univ. of Florida,Gainesville, FL 32611, USA.)
Abstract	Respiratory muscle weakness resulting from both diaphragmatic contractile dysfunction and atrophy has been hypothesized to contribute to the weaning difficulties associated with prolonged mechanical ventilation (MV). While it is clear that oxidative injury contributes to MV-induced diaphragmatic weakness, the source(s) of oxidants in the diaphragm during MV remain unknown. These experiments tested the hypothesis that xanthine oxidase (XO) contributes to MV-induced oxidant production in the rat diaphragm and that oxypurinol, a XO inhibitor, would attenuate MV-induced diaphragmatic oxidative stress, contractile dysfunction, and atrophy. Adult female Sprague-Dawley rats were randomly assigned to one of six experimental groups: 1) control, 2) control with oxypurinol, 3) 12 h of MV, 4) 12 h of MV with oxypurinol, 5) 18 h of MV, or 6) 18 h of MV with oxypurinol. XO activity was significantly elevated in the diaphragm after MV, and oxypurinol administration inhibited this activity and provided protection against MV-induced oxidative stress and contractile dysfunction. Specifically, oxypurinol treatment partially attenuated both protein oxidation and lipid peroxidation in the diaphragm during MV. Further, XO inhibition retarded MV-induced diaphragmatic contractile dysfunction at stimulation frequencies >60 Hz. Collectively, these results suggest that oxidant production by XO contributes to MV-induced oxidative injury and contractile dysfunction in the diaphragm. Nonetheless, the failure of XO inhibition to completely prevent MV-induced diaphragmatic oxidative damage suggests that other sources of oxidant production are active in the diaphragm during prolonged MV.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
DOI	10.1152/japplphysiol.91106.2008
Journal	Journal of Applied Physiology
Issue Number	2
Volume Number	106
Language	English
Publisher	American Physiological Society
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Diaphragm Physiopathology Muscle Contraction Muscle Weakness Muscular Atrophy Oxidative Stress Ventilator-induced Lung Injury Xanthine Oxidase Metabolism Animals Drug Effects Enzymology Disease Models, Animal Electric Stimulation Enzyme Inhibitors Pharmacology Hypoxanthine Lipid Peroxidation Prevention & Control Oxypurinol Protein Carbonylation Rats, Sprague-dawley Time Factors Uric Acid Drug Therapy Xanthine Xanthine Dehydrogenase Antagonists & Inhibitors Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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