Do ischemia, noise and cisplatin cause cochlear vascular damage?

Deafness is one of the most commonly diffused disabilities because of increasing people age and environmental noise levels. Hearing damage caused by age, noise or ototoxic drugs is generally irreversible since cochlear neurons and hair cells are not able to regenerate. Noise-induced hearing loss and ototoxic drugs are significant sources of hearing impairment among humans. The causing mechanisms can be attributed to: direct mechanical damage and damage caused by metabolic stress, mediated by an increased of the oxidative metabolism in the inner ear. It has already been observed that routine blood pressure values recorded in young adult patients complaining of sudden sensorineural hearing loss have been significantly lower when compared with those of an age-matched control group, thus indicating a possible role of hypothension in the genesis of inner ear disorders. For the study of sudden hearing loss, in literature are available several in vivo protocols for deafening noise and ototoxic drugs and few in vitro for hipoxic damage. This research aims to develop in rat model, the techniques to induce damages to inner ear following ischemic events like hypoxia, deafening noise or cisplatin toxicity, and to investigate in deep the amount of damage. The preliminary histological results allowed us to detect a specific protein expression profile in relation to the tissue oxidation (HIF-1á, p-JNK) and cardiovascular disease (TM and TF). This profile, in conclusion, shows a correlation among the three different hearing loss damages: they cause vascular damage.