• F Watanabe, K Koga, N Hakuba, and K Gyo.
• Department of Otolaryngology, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, 791-0295, Japan. hakubax@m.ehime-u.ac.jp
• Neuroscience. 2001 Jan 1; 102 (3): 639-45.

AbstractThe effects of hypothermia on ischemia-reperfusion injury of the cochlea were studied in gerbils. Hearing was assessed by sequentially recording compound action potentials before, during and after the ischemia. The degree of hair cell loss in the organ of Corti was evaluated in specimens stained with rhodamine-phalloidin and the dye Hoechst 33342. Ischemic insult was applied to the animals by occluding the bilateral vertebral arteries for 15 min under normothermic or hypothermic (rectal temperature 32 degrees C) conditions. Interruption of the blood supply to the cochlea caused a tremendous increase in the compound action potential threshold, which usually recovered to some extent with reperfusion. In the ischemia/normothermic group, the threshold did not return to the pre-ischemic level. The average increase in the threshold seven days after ischemia was 20.0 dB. Histologically, the hair cell loss increased gradually until four days after the ischemic insult. On the seventh day, the mean loss of inner and outer hair cells at the basal turn was 31.1 % and 2.4 %, respectively. In the ischemia/hypothermic group, the threshold returned to the pre-ischemic level within 30 min after reperfusion and remained stable thereafter. The mean loss of inner and outer hair cells on the seventh day was 0.1 % and 0.2 %, respectively. These results indicate that hypothermia can prevent inner ear damage, which otherwise occurs after transient ischemia of the cochlea.

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