Tympanic membrane vessel revisited: a study in an animal model
2003 (English)In: Otology and Neurotology, ISSN 1531-7129, E-ISSN 1537-4505, Vol. 24, no 3, 494-499 p.Article in journal (Refereed) Published
HYPOTHESIS: The present study aimed at elucidating whether there are blood vessels in the semitransparent portion of the tympanic membrane.
BACKGROUND: The normal semitransparent portions of pars tensa show strikingly few, small-caliber vessels under the otomicroscope. The major portion of a pars tensa seems to be devoid of blood vessels. In inflammatory conditions of the middle ear, the vascular pattern of the tympanic membrane is dramatically altered, and blood vessels traversing the pars tensa can be discernable.
METHODS: The study was performed in rats with healthy tympanic membranes and in tympanic membranes obtained from animals with purulent otitis media evoked by inoculation of Str. pneumoniae. The tympanic membrane vessels were dilated by injection of adenosin, and directly afterwards the animal was perfused with china ink. Vessels were also revealed by immunohistochemistry with antibodies for Thy-1 and the von Willebrand factor as well as by detection of carbon particles at an ultrastructural level.
RESULTS: Adenosin caused a marked dilation of the mallear and annular vessels. However, no preexisting vasculature was revealed in the normally transparent portions of the pars tensa except single vessels in the posterior quadrant and in the lower quadrants. In Str. pneumoniae-induced acute otitis media, the tympanic membrane thickened, bulged, and discolored. Even then, at 12 hours after inoculation, no vessels could be distinguished in the normally transparent portions of the tympanic membrane. However, at 4 and 7 days of acute purulent otitis media, vessels developed in those areas, most probably through ingrowth of newly formed vessels.
CONCLUSION: The results support the view that the semitransparent portions of the pars tensa lack vascularity. In inflammation, new vessels are formed in pars tensa to meet the demand for an increased blood supply.
Place, publisher, year, edition, pages
2003. Vol. 24, no 3, 494-499 p.
IdentifiersURN: urn:nbn:se:umu:diva-37255PubMedID: 12806306OAI: oai:DiVA.org:umu-37255DiVA: diva2:358609