To elucidate the mechanisms of epithelial mucus hypersecretion in upper respiratory airway inflammation, we produced hypertrophic and metaplastic changes of goblet cells in rat nasal respiratory epithelium by intranasal instillation of endotoxin. Significant increase of hypertrophic goblet cells was induced in the septal epithelium transversely sectioned at the level of incisive papilla at 24 h after the intranasal instillation of 0.1 mg of endotoxin. This change was completed after 3 d of endotoxin instillations and recovered by normal epithelium 7 d after the last instillation. Total cell number and the number of basal and ciliated cells counted over 2 mm of basal lamina did not change; however, the number of goblet cells increased and that of nongranulated secretory cells decreased time-dependently after endotoxin instillations. Mitotic rates examined after a 6-h colchicine metaphase blockade were very low at any time point studied, and cell division did not play a major role in this process. These results indicate that endotoxin induces hypertrophic and metaplastic changes of goblet cells in rat nasal epithelium rather than a hyperplastic change, and this metaplasia is produced by direct conversion of nongranulated secretory cells into the goblet cells. Histochemical examination of this epithelium revealed that most of the mucus produced by these goblet cells was sulfomucin. Intraperitoneal injection of antirat neutrophil antiserum or cyclophosphamide depleted circulating blood neutrophils. Endotoxin-induced changes of goblet cells were significantly inhibited in these neutrophil-depleted rats, and intranasal instillation of elastase also induced hypertrophic and metaplastic changes of goblet cells.
We produced hypertrophic and metaplastic changes of goblet cells in rat nasal respiratory epithelium by the intranasal instillation of endotoxin (ETN). In the present study, we examined in vivo effects of indomethacin (IND), dexamethasone (DEX), and erythromycin (EM) on intraepithelial mucus production using this animal model. Intraperitoneal injection of IND (2 to 4 mg/kg body weight x 4 days) or DEX (4 to 8 mg/kg body weight x 4 days) significantly inhibited intraepithelial mucus production induced after 3 days of ETN instillations. Intraperitoneal injection of EM (100 mg/kg body weight x 8 days), aminobenzylpenicillin (ABPC, 200 mg/kg body weight x 8 days), and cephalothin (CET, 200 mg/kg body weight x 8 days) also inhibited intraepithelial mucus production induced after 7 days of ETN instillations. When compared with ABPC and CET, EM had a greater inhibitory effect. These results indicate that ETN-induced intraepithelial mucus production can be inhibited by treatment with the anti-inflammatory drugs IND and DEX. Antibiotics such as EM, ABPC, and CET will also be effective, probably by preventing secondary bacterial infection, and EM has an additional inhibitory effect on intraepithelial mucus production.
In the present study, hypertrophic and metaplastic changes of goblet cells were induced in rat nasal epithelium by intranasal instillation of endotoxin or elastase. A significant increase in the amount of intraepithelial mucosubstance was observed after 24 hours during 3 days of instillation. The elastase-induced mucus production was not inhibited in neutrophil-depleted rats, but the endotoxin-induced change was significantly inhibited. Intranasal instillation of the neutrophil elastase inhibitor ONO-5046 partially inhibited the endotoxin-induced mucus production. Epithelial mucus secretion was evaluated by the temporary decrease in the amount of intraepithelial mucosubstance. The endotoxin-induced mucus secretion peaked 3 to 6 hours after intranasal instillation, coinciding with the peak of the intraepithelial neutrophil infiltration. The elastase-induced mucus secretion peaked 1 to 3 hours after intranasal instillation; intraepithelial neutrophil infiltration was not induced by elastase. These results indicate that neutrophil elastase is an important mediator of the intraepithelial mucus synthesis and secretion induced by endotoxin.
Six patients with intractable epistaxis from the posterior nasal cavity which could not be controlled by conventional packing method are reported. The four men and two wemen were 54 to 75 years of age (mean, 64 years). The site of bleeding was confirmed by angiography by Seldinger's procedure through the femoral artery at the groin or a cut-down approach through the superficial temporal artery. The maxillary artery, which was suspected to be the site of bleeding, was successfully embolized with small pieces of Gelfoam® and a few coils. No further epistaxis or complications of the embolism occurred. Super-selective intraarterial embolization is a new and effective therapy for intractable severe epistaxis.
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