title: Cochlear microperfusion: experimental evaluation of a potential new therapy for severe hearing loss caused by inflammation.
abstract: OBJECTIVE
  Cochlear microperfusion will be a useful treatment of severe sensorineural hearing loss caused by inflammation.
  
  
  BACKGROUND
  Viruses, bacteria, and autoimmunity can initiate inflammation in the inner ear. The acute phase is associated with elevations in cytokines, nitrous oxide, and cellular infiltrates and the breakdown of the blood-labyrinthine barrier. The chronic phase leads to irreversible ossification of the labyrinth.
  
  
  METHODS
  The authors developed cochlear microperfusion to facilitate removal of inflammatory cells and their byproducts during the acute phase of inflammation. Using a ventral approach to the guinea pig cochlea, the authors displaced resident perilymph by delivering perfusate into the scala vestibuli and collecting the effluent from the scala tympani. The authors evaluated the benefit of the procedure in an animal model of severe hearing loss caused by inflammation.
  
  
  RESULTS
  Healthy controls undergoing cochlear microperfusion with phosphate-buffered saline incurred a mean hearing loss of 16 dB (n=4). This hearing loss was associated with the creation of two cochleostomies and not the perfusion itself. Sterile labyrinthitis (n=5) generated by perfusion of the cochlea with antigen consistently produced severe hearing loss over the initial 48 hours, and this hearing loss persisted for the subsequent 7 days. Therapeutic cochlear microperfusion, performed within the first 24 hours of developing severe hearing loss (n=9), immediately restored on average 24 dB (p <0.007) of hearing.
  
  
  CONCLUSIONS
  Cochlear microperfusion is a promising new technique for treating severe deafness caused by inflammation. The benefit may be sustained when combined with local delivery of immunosuppressive agents to the inner ear.
authors.affiliation: Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of California, San Diego, School of Medicine, 92103-8895, USA.
authors.forename: Gregory C
authors.initials: GC
authors.lastname: Barkdull
authors.forename: Cong
authors.initials: C
authors.lastname: Vu
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Keithley
authors.forename: Jeffrey P
authors.initials: JP
authors.lastname: Harris
mesh_terms: D000818:Animals; D001309:Auditory Threshold / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D003051:Cochlea / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006168:Guinea Pigs; D006319:Hearing Loss, Sensorineural / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D006433:Hemocyanins; D018836:Inflammation Mediators / Q000378:metabolism; D007762:Labyrinthitis / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D007962:Leukocytes; D010477:Perfusion / Q000379:methods*; D010586:Phagocytes / Q000276:immunology; D012533:Scala Tympani / Q000276:immunology / Q000473:pathology
chemical_list: D018836:Inflammation Mediators; D006433:Hemocyanins; C032808:keyhole-limpet hemocyanin