The effect of mannitol upon cochlear dysfunction induced by transient local anoxia

Transient local anoxia of the cochlea was induced by pressing the labyrinthine artery, and compound action potential (CAP) or endocochlear potential (EP) was measured before and after transient local anoxia ranging from 5 to 60 min using 106 albino guinea pigs. The complete interruption of the cochlear blood flow by this procedure and its full restoration after releasing the pressure on the artery was confirmed by a laser-Doppler flowmeter. The anoxia of less than 10 min induced no post-anoxic cochlear dysfunction, whereas the anoxia of a longer duration induced an irreversible dysfunction of the cochlea. It was evident that the post-anoxic recovery of the CAP threshold was worse as the anoxia period was prolonged, and CAP was almost completely abolished after 60-min anoxia. In animals which were administered mannitol intravenously just after the restoration of the cochlear blood circulation, the recovery of the CAP threshold was significantly better than that in the control animals, when the animals were subjected to local anoxia of 15- to 30-min duration. No beneficial effect, however, was observed in the 60-min anoxia group. In conclusion, local anoxia of 10 min or longer caused cochlear dysfunction, which was partially but significantly alleviated by mannitol.