title: Ischemia of the endolymphatic sac.
abstract: A decrease in vascular density in the endolymphatic sac was suspected as a factor in the pathogenesis of endolymphatic hydrops in Meniere's disease. The present study was undertaken to explore this possibility by cutting the posterior meningeal artery and the sigmoid sinus above and below the external aperture of the vestibular aqueduct or by incision of the dura adjacent to the sinus in 18 guinea pigs. The lesions in the sac were greater in the segmental ablation of the artery and sinus and were consistently associated with the development of endolymphatic hydrops. Among the lesions shown in the sac epithelia, the intermediate portion was most often and most severely affected with a decrease in rugose formation and a flattening of the tall epithelial cells or replacement of epithelial cells by squamous type cells. A high correlation between the lesions in the intermediate portion and occurrence of hydrops suggests that the intermediate portion plays a greater role in the pathogenesis of endolymphatic hydrops. The sac luminal precipitates known to be increased in human Meniere's cases were decreased or absent in this study, which suggests that the increased amount is unlikely to be the cause of endolymphatic hydrops. The evidence supports the hypothesis that these substances are secreted by the endolymphatic sac. The limited sensory cell lesions seen in the cochleae and saccules are likely to be due to a temporary vascular ischemia and endolymphatic hydrops.
authors.affiliation: Department of Otolaryngology, Guro Hospital, Korea University, Seoul.
authors.forename: K S
authors.initials: KS
authors.lastname: Lee
authors.forename: R S
authors.initials: RS
authors.lastname: Kimura
mesh_terms: D000818:Animals; D004487:Edema / Q000209:etiology* / Q000473:pathology; D004710:Endolymph; D004712:Endolymphatic Sac / Q000098:blood supply* / Q000473:pathology; D006168:Guinea Pigs; D007511:Ischemia / Q000150:complications* / Q000473:pathology; D015837:Vestibular Diseases / Q000209:etiology* / Q000473:pathology