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Trans-Tympanic Drug Delivery for the Treatment of Ototoxicity

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Hyperbaric oxygen upregulates cochlear constitutive nitric oxide synthase.

Chia-Der Lin¹, I-Hua Wei, Chih-Ho Lai

¹Department of Otolaryngology-Head and Neck Surgery, China Medical University Hospital, and Graduate Institute of Clinical Medical Science, Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.

BMC Neuroscience

|February 24, 2011

Summary

Hyperbaric oxygen therapy (HBOT) may increase nitric oxide synthase (NOS) expression in the cochlea but does not harm auditory function or morphology. This study investigated HBOT effects on guinea pig ears, finding no significant hearing changes.

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Area of Science:

Oto-rhino-laryngology
Hyperbaric Medicine
Cellular Biology

Background:

Hyperbaric oxygen therapy (HBOT) is used for inner ear diseases, but its role in cochlear conditions is debated.
Limited research exists on cellular changes in the inner ear following HBOT.
Nitric oxide (NO) is a key signaling molecule in cochlear physiology and pathology, synthesized by nitric oxide synthase (NOS).

Purpose of the Study:

To investigate the effects of repetitive HBOT on eardrum morphology.
To assess cochlear function after HBOT using auditory brainstem responses.
To examine the expression of NOS isoforms in cochlear substructures post-HBOT.

Main Methods:

Repetitive hyperbaric oxygen therapy (HBOT) was administered to guinea pigs.
Eardrum morphology was evaluated.
Tone burst auditory brainstem responses were used to measure hearing thresholds.
Immunohistochemistry was employed to detect NOS isoform expression in cochlear substructures.

Main Results:

Minor eardrum changes were observed, with no significant hearing threshold shifts.
Constitutive NOS (nNOS and eNOS) expression was upregulated in cochlear substructures.
Inducible NOS was not detected in either normal or HBOT-treated animals.
No significant DNA fragmentation was observed, indicating no widespread cell death.

Conclusions:

The standard HBOT protocol can increase constitutive NOS expression in the cochlea.
This upregulation of NOS does not lead to cell death or affect cochlear morphology.
Auditory function remains unchanged following the customary HBOT protocol.