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JÖRGEN FALBE-HANSEN, M.D.; ERNA CHRISTENSEN, M.D.; LENNART GISSELSSON, M.D.; HANS J. HANSEN, M.D.; PER M. PERMIN, M.D.

AMA Arch Otolaryngol. 1958;67(1):71-77.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

According to numerous studies the cochlear microphonic response appears to arise in the sensory cells of the organ of Corti (Guttman and Barrera; Neff, Wever, and Neff; Juul and Vraa-Jensen; Rüedi et al.; Larsell et al., and Békésy). If the hair cells are destroyed, the microphonic response disappears, and, if their vitality is reduced, e. g., by severe oxygen deprivation, the microphonic response is diminished. If the oxygen deprivation is carried very far, or if the animal is exposed to repeated experiments of oxygen deprivation, the microphonic response will become lowered to one-fifth of the original magnitude. If the animal is again supplied with a normal amount of oxygen, the microphonic response does not return to the initial value during the few hours that such experiments are continued (Lawrence and Wever; Gisselsson). There is no doubt that the severe anoxia has given rise to severe changes in the acoustic organ. . . . [Full Text PDF of this Article]

Author Affiliations
Cophenhagen; Lund, Sweden; Copenhagen

From the Ear Clinic, Kommunehospitalet, Copenhagen, Denmark, and the University Ear Clinic, Lund, Sweden.

Footnotes
Accepted for publication March 8, 1957.

This study was aided by a grant from the P. Carl Petersen Foundation.

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