Effects of Hypothermia on Prevention of Hearing Loss Produced by Transient Cochlear Ischemia in Gerbils.

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  • 虚血性内耳障害に対する低体温の効果　　スナネズミ内耳虚血モデルにおける検討
  • ―スナネズミ内耳虚血モデルにおける検討―

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Abstract

Using gerbils, the effects of hypothermia on ischemia-reperfusion injury of the cochlea were studied. Under normothermic or hypothermic (rectal temperature 32°C) conditions, cochlear ischemia was created by occluding the bilateral vertebral arteries for 15 minutes in gerbils, which lack the posterior cerebral communicating arteries since the labyrinthine arteries are nourished solely by the vertebral arteries. Hearing was evaluated by recording cochlear compound action potentials (CAPS) following the ischemia. Occlusion of the arteries caused a marked increase in the CAP threshold, which usually recovered to some extent with reperfusion. In the ischemia-normothermic group, the CAP threshold did not return to the pre-ischemic level. The mean increase in the threshold 7 days after ischemia was 16.3dB. In the ischemia-hypothermic group, the CAP threshold returned to the pre-ischemic level within 30 minutes after reperfusion, and remained stable thereafter. Histologically, the degree of hair cell death in the organ of Corti was evaluated by F-actin and DNA staining methods. In the ischemia-normothermic group, the hair cell loss increased gradually until 4 days after the ischemic insult. On the 7th day, the mean loss of inner and outer hair cells (IHCs and OHCs) at the basal turn was 26.4% and 2.9%, respectively. On the other hand, the mean losses of the IHCs and OHCs after the ischemia were less than 0.3% in the ischemia-hypothermic group. These findings suggest that hypothermia completely prevented the hearing loss caused by ischemia-reperfusion injury of the cochlea.

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