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Open Access Highly Accessed Research article

Hyperbaric oxygen upregulates cochlear constitutive nitric oxide synthase

Chia-Der Lin12, I-Hua Wei3, Chih-Ho Lai4, Te-Chun Hsia5, Ming-Ching Kao67, Ming-Hsui Tsai12, Ching-Hsiang Wu38 and Mang-Hung Tsai3*

Author Affiliations

1 Department of Otolaryngology-Head and Neck Surgery, China Medical University Hospital, Taichung, Taiwan

2 Graduate Institute of Clinical Medical Science, School of Medicine, China Medical University, Taichung, Taiwan

3 Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan

4 Department of Microbiology, School of Medicine, China Medical University, Taichung, Taiwan

5 Hyperbaric Oxygen Therapy Center, China Medical University Hospital, Taichung, Taiwan

6 Department of Biological Science and Technology, College of Life Sciences, China Medical University, Taichung, Taiwan

7 Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan

8 Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan

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BMC Neuroscience 2011, 12:21  doi:10.1186/1471-2202-12-21

Published: 22 February 2011

Abstract

Background

Hyperbaric oxygen therapy (HBOT) is a known adjuvant for treating ischemia-related inner ear diseases. Controversies still exist in the role of HBOT in cochlear diseases. Few studies to date have investigated the cellular changes that occur in inner ears after HBOT. Nitric oxide, which is synthesized by nitric oxide synthase (NOS), is an important signaling molecule in cochlear physiology and pathology. Here we investigated the effects of hyperbaric oxygen on eardrum morphology, cochlear function and expression of NOS isoforms in cochlear substructures after repetitive HBOT in guinea pigs.

Results

Minor changes in the eardrum were observed after repetitive HBOT, which did not result in a significant hearing threshold shift by tone burst auditory brainstem responses. A differential effect of HBOT on the expression of NOS isoforms was identified. Upregulation of constitutive NOS (nNOS and eNOS) was found in the substructures of the cochlea after HBOT, but inducible NOS was not found in normal or HBOT animals, as shown by immunohistochemistry. There was no obvious DNA fragmentation present in this HBOT animal model.

Conclusions

The present evidence indicates that the customary HBOT protocol may increase constitutive NOS expression but such upregulation did not cause cell death in the treated cochlea. The cochlear morphology and auditory function are consequently not changed through the protocol.