title: Sensorineural hearing loss and ischemic injury: Development of animal models to assess vascular and oxidative effects.
abstract: Hearing loss may be genetic, associated with aging or exposure to noise or ototoxic substances. Its aetiology can be attributed to vascular injury, trauma, tumours, infections or autoimmune response. All these factors could be related to alterations in cochlear microcirculation resulting in hypoxia, which in turn may damage cochlear hair cells and neurons, leading to deafness. Hypoxia could underlie the aetiology of deafness, but very few data about it are presently available. The aim of this work is to develop animal models of hypoxia and ischemia suitable for study of cochlear vascular damage, characterizing them by electrophysiology and gene/protein expression analyses. The effects of hypoxia in infarction were mimicked in rat by partial permanent occlusion of the left coronary artery, and those of ischemia in thrombosis by complete temporary carotid occlusion. In our models both hypoxia and ischemia caused a small but significant hearing loss, localized at the cochlear apex. A slight induction of the coagulation cascade and of oxidative stress pathways was detected as cell survival mechanism, and cell damages were found on the cuticular plate of outer hair cells only after carotid ischemia. Based on these data, the two developed models appear suitable for in vivo studies of cochlear vascular damage.
authors.affiliation: Bioacoustics Research Laboratory, Department of Neurosciences, University of Padua, 35129 Padua, Italy. Electronic address: elena.olivetto@unipd.it.
authors.forename: E
authors.initials: E
authors.lastname: Olivetto
authors.affiliation: Bioacoustics Research Laboratory, Department of Neurosciences, University of Padua, 35129 Padua, Italy. Electronic address: edi.simoni@unipd.it.
authors.forename: E
authors.initials: E
authors.lastname: Simoni
authors.affiliation: Bioacoustics Research Laboratory, Department of Neurosciences, University of Padua, 35129 Padua, Italy. Electronic address: valeria.guaran@unipd.it.
authors.forename: V
authors.initials: V
authors.lastname: Guaran
authors.affiliation: Bioacoustics Research Laboratory, Department of Neurosciences, University of Padua, 35129 Padua, Italy. Electronic address: laura.astolfi@unipd.it.
authors.forename: L
authors.initials: L
authors.lastname: Astolfi
authors.affiliation: Bioacoustics Research Laboratory, Department of Neurosciences, University of Padua, 35129 Padua, Italy; ENT Surgery, Department of Neurosciences, University of Padua, 35129 Padua, Italy. Electronic address: alessandromartini@unipd.it.
authors.forename: A
authors.initials: A
authors.lastname: Martini
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D001777:Blood Coagulation; D002545:Brain Ischemia / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D016893:Carotid Stenosis / Q000150:complications*; D003051:Cochlea / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D023921:Coronary Stenosis / Q000150:complications*; D004195:Disease Models, Animal; D016057:Evoked Potentials, Auditory, Brain Stem; D005786:Gene Expression Regulation; D006319:Hearing Loss, Sensorineural / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008833:Microcirculation; D018384:Oxidative Stress; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow; D015398:Signal Transduction
chemical_list: D015415:Biomarkers