title: Sarthran preserves cochlear microcirculation and reduces temporary threshold shifts after noise exposure.
abstract: The cause of noise-induced hearing loss remains unclear despite years of both epidemiologic and experimental investigation. Among the many possible pathophysiologic mechanisms that may contribute to noise-induced temporary or permanent threshold shifts are insufficiencies in cochlear blood flow. Although the literature is inconsistent, several histologic and physiologic studies demonstrate signs of reduced circulation in the cochlea after noise exposure. Recent studies using computer-enhanced intravital microscopy complement these earlier findings. Evidence suggests that these microcirculatory events are mediated in part by several circulating factors, including the potent vasoactive peptide angiotensin. This study investigated this possibility by pretreating with the angiotensin receptor antagonist sarthran during noise exposure and examining both cochlear microcirculation and auditory sensitivity. The results of these experiments show noise-induced ischemia in the lateral wall of the cochlea and temporary threshold shifts. Treatment with sarthran prevented this noise-induced microcirculatory ischemia and preserved auditory sensitivity at the low frequencies tested. These findings support a role for the angiotensinergic system during noise exposure and suggest that preservation of cochlear blood flow is functionally related to auditory sensitivity.
authors.affiliation: Department of Otolaryngology, Wayne State University, Detroit, Michigan 48201, USA.
authors.forename: B
authors.initials: B
authors.lastname: Goldwin
authors.forename: M J
authors.initials: MJ
authors.lastname: Khan
authors.forename: B
authors.initials: B
authors.lastname: Shivapuja
authors.forename: M D
authors.initials: MD
authors.lastname: Seidman
authors.forename: W S
authors.initials: WS
authors.lastname: Quirk
mesh_terms: D000161:Acoustic Stimulation; D000200:Action Potentials / Q000187:drug effects; D000704:Analysis of Variance; D000804:Angiotensin II / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001309:Auditory Threshold / Q000187:drug effects*; D001783:Blood Flow Velocity; D003051:Cochlea / Q000098:blood supply* / Q000187:drug effects; D003055:Cochlear Microphonic Potentials / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004912:Erythrocytes / Q000502:physiology; D006168:Guinea Pigs; D006317:Hearing Loss, Noise-Induced / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D007091:Image Processing, Computer-Assisted; D007511:Ischemia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D017078:Laser-Doppler Flowmetry; D008297:Male; D008833:Microcirculation / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D008853:Microscopy; D009622:Noise / Q000009:adverse effects*; D012039:Regional Blood Flow / Q000187:drug effects; D012815:Signal Processing, Computer-Assisted; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology*; D014743:Videotape Recording
chemical_list: D057911:Angiotensin Receptor Antagonists; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; C014805:angiotensin II, Sar(1)-Thr(8)-