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Hyperbaric oxygen treatment following mid‐cervical spinal contusion injury ‐ diaphragm outcomes
Author(s) -
Turner Sara M,
Schuster Cassandra M,
Morton Aaron B,
Hinkley J. Matthew,
Fuller David D,
Smuder Ashley J
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.873.5
Subject(s) - oxidative stress , atrophy , medicine , diaphragm (acoustics) , skeletal muscle , muscle atrophy , reactive oxygen species , sarcopenia , spinal cord injury , spinal cord , endocrinology , pathology , biology , biochemistry , physics , psychiatry , acoustics , loudspeaker
Oxidative damage to the diaphragm as a result of cervical spinal cord (cSCI) injury promotes muscle atrophy. However, prevention of cSCI‐induced oxidative stress in the diaphragm via antioxidant therapy can reduce diaphragm atrophy. Hyperbaric oxygen treatment (HBOT) can modulate expression of reactive oxygen species (ROS) and antioxidant enzymes in skeletal muscle. Although mounting evidence suggests HBOT exposure acutely following spinal cord injury (SCI) is associated with a small but functionally beneficial impact on spinal cord pathology, the impact of HBOT on skeletal muscles after SCI is unknown. We tested the hypothesis that HBOT exposure initiated immediately following cervical SCI would alter the expression of diaphragm genes and proteins related to oxidative stress and skeletal muscle atrophy. Rats were randomly divided into the following groups: 1) naïve (no prior treatment), 2) lateral contusion at C3/4 (cSCI) and, 3) cSCI + daily HBOT. The HBOT consisted of a 1‐hr exposure to 2.0 atmospheres of 100% O 2 , beginning on the day of SCI and continuing for 10‐days. After the 10 th treatment day, diaphragm muscle was harvested for analyses of mRNA and protein expression related to muscle proteolysis, oxidative stress, and mitochondrial function. Compared to naïve rats, the cSCI cohort showed increased expression (p<0.05) of markers related to atrophy (Atrogin‐1, MuRF‐1, IL‐1, TWEAK), oxidative stress (ROS, 4‐HNE), and mitochondrial dysfunction (decreased respiratory chain ratio; RCR). The cohort of cSCI rats treated with daily HBOT had significantly lower expression of the markers of proteolysis and oxidative stress, and a significantly greater RCR compared to untreated cSCI rats (p<0.05). In addition, daily HBOT increased antioxidant enzyme expression (SOD2, GPX1). Our data show that daily HBOT has a substantial impact on the diaphragmatic response to cervical SCI. In particular, the reduction in atrophy‐related gene expression raises the possibility that HBOT may have value as an adjunctive therapy to promote health in the phrenic neuromuscular system following cervical SCI. Support or Funding Information Craig H. Neilsen Foundation 313369 (SMFT); 1 R01 NS080180‐01A1 (DDF), State of Florida Brain and Spinal Cord Injury Research Program (DDF)