Volume 117, Issue 2 pp. 194-198
Article

A Potential Portal Flow in the Inner Ear

Morten Friis MD

Corresponding Author

Morten Friis MD

Department of Otolaryngology, Head & Neck Surgery, Rigshospitalet, Denmark

Department of Medical Anatomy, The Panum Institute, Copenhagen, Denmark

Inner Ear Research Centre, University of Copenhagen, Copenhagen, Denmark.

Morten Friis, MD, Department of Otolaryngology, Head and Surgery, University of Copenhagen, F2071, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.Search for more papers by this author
Klaus Qvortrup MD, PhD

Klaus Qvortrup MD, PhD

Department of Otolaryngology, Head & Neck Surgery, Rigshospitalet, Denmark

Department of Medical Anatomy, The Panum Institute, Copenhagen, Denmark

Inner Ear Research Centre, University of Copenhagen, Copenhagen, Denmark.

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First published: 02 January 2009
Citations: 18

This study was supported by Desirée og Niels Ydes Fond, The Schioldann′s Foundation, Landsforeningen for Bedre Hørelse/Menieré og Tinnitus Foreningen.

Abstract

Objectives/Hypothesis: The aim of the present study was to visualize the flow direction of blood in the extraosseous part of the vein of the vestibular aqueduct (VVA) and to explore the effect of an induced obstruction in the distal part of the VVA before it merges with the sigmoid sinus. The endolymphatic sac has been implicated as a potential endocrine gland, which venules drain to the VVA. A reversal of the direction of flow in the VVA toward the inner ear could, through vestibular arteriovenous anastomosis, cause portal circulation in the inner ear.

Study Design: The authors conducted an experimental animal study using in vivo fluorescence microscopy.

Results: Obstructing the distal part of the VVA just before it empties into the sigmoid sinus immediately reverses the flow of blood in the VVA toward the inner ear.

Conclusions: After an obstruction of the VVA, the drained venous blood from the endolymphatic sac may enter a portal circulation in the inner ear, which could cause disturbances in the endolymph homeostasis and potentially symptoms as seen in Meniere disease.

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