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KMID : 0361019980410091127
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Korean Journal of Otolaryngology - Head and Neck Surgery
1998 Volume.41 No. 9 p.1127 ~ p.1132
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Platelet Activating Factor Induced Maxillary Sinusitis in Rabbits
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정필섭/Pil Seob Jeong
이정구/전시영*/Chung Ku Rhee/Sea Yuong Jeon*
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Abstract
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Background: Platelet activating factor (PAF) has been known to implicate one of potent inflammatory mediators and is reported to be involved in many pathologic processes, especially in inflammation and allergy. PAF has induced cytotoxic
effets on
the human paranasal sinus mucosa in vitro, showing ciliary inhibition, ciliostasis and cellular damage to the mucosal epithelium, in both dose and time dependent manners. However, the exact role of PAF in the pathogenesis of sinusitis is not yet
known.
Objective: The purpose of this study was to provide a new model of acute sinusitis by application of PAF into the maxillary sinus in rabbits. Materials and Methods: Rabbits were divided into 2 groups. Experimental groups were
applied
with
16 ㎍/㎖ of PAF into the maxillary sinus percutaneously. Control groups were applied with normal saline using the same technique as in the experimental groups. The presence of purulent secretion wa observed in the nostril of rabbits, and the
culture and
smears of the secretions were performed. All of the mucosae were taken from the inferomedial wall of each sinus for light microscopy. Results: Mucoid and purulent discharges were observed in rabbits of the experimental groups at 5 and 7
days
after the application of PAF, respectively. Pasteurella multocida was found in the sinus content of experimental groups at 5 and 7 days. The prominent epithelial disruption and the infiltration of the inflammatory cells (predominantly
eosinophils)
into
the epithelium and lamina propria were observed at 7 days in PAF-applied group. Conclusion: In this study, PAF induced sinusitis without occlusion of the natural ostium of the maxillary sinus in rabbits, therby providing another animal
model
of
sinusitis for the understanding of the pathogenesis of sinusitis caused by inflammatory mediators.
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KEYWORD
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