Experimental study of transient cochlear ischemi a as acause of sudden deafness

摘要

The etiology of sudden deafness or idiopathic suddensensorineural hearing loss （ISSHL） remains unclear.Over the past 15 years, we have investigated themechanisms of ischemic-induced hearing loss usinga gerbil model of transient cochlear ischemia. In thegerbil, cochlear ischemia can be induced by occludingthe bilateral vertebral arteries simultaneously at theneck, because the posterior communicating arteries ofthe Circle of Willis close spontaneously around 1 moafter birth. When 15 min ischemia was loaded on thisanimal, permanent hearing loss of about 25 dB andthe death of hair cells, especially inner hair cells wereinduced. These pathological changes were mainly dueto lack of an energy source, glutamate excitotoxicity,and the production of free radicals, especially superoxideand nitrous oxide species. Ischemic damage couldbe prevented by various procedures, such as coolingthe cochlea, intratympanic administration of insulin-likegrowth factor 1 or AM-111 （an anti-apoptotic agent）,and systemic administration of prednisolone （steroid）,edarabone （free radical scavenger）, ginsenoside Rb1（Kanpo）, hematopoietic stem cells, glia-cell derivedneurotrophic factor, and liposome-encapsulated hemoglobin（artificial red blood cells）. We also found that thecochlea was protected by the ischemic tolerance, indicating catingthat minor cochlear ischemia alleviates or preventsinner ear damage in subsequent severe cochlearischemia. As ISSHL usually occurs suddenly, with nopreceding sign or symptom, we suggest that most ISSHLcases are caused by circulatory disturbance, probablyat the stria vascularis.