Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The site of leakage in middle ear vessels was determined and characterized in experimental otitis media in rats. Middle ear effusion was induced by intravenous administration or local application in the tympanic bulla of substance P (SP), acetylcholine, and histamine. In another experiment, a 14 degrees C airstream was blown into the external auditory canal. Colloidal carbon was used to trace leakage sites at the light and electron microscopic levels. All mediators tested and the 14 degrees C airstream resulted in an increased number of leaking vessels in the pars flaccida and the middle ear mucosa. The leakage sites were restricted to capillaries and postcapillary venules. Increased numbers of degranulated pars flaccida mast cells were observed for SP only. Interendothelial gaps formed in leakage vessels after administration of mediators and stimulation of the external auditory canal with a 14 degrees C airstream. Also, cytoplasmic vesicle-like structures within the endothelial cells increased in number following SP and histamine treatment, suggesting that an increased permeability in experimental otitis media does not occur exclusively through interendothelial gaps.
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PMID:Identification and characterization of middle ear vascular leakage sites in experimental otitis media. 169 67

The mucosal lining of the middle ear cavity, in particular that of the tympanic membrane and its pars flaccida, exhibits a number of sensory nerves containing the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP). The mucosa is not only rich in nerves and blood vessels but also contains numerous mast cells. It is possible that interactions between histamine-containing mast cells and SP-containing and CGRP-containing nerves--neurogenic inflammation--is one of the mechanisms involved in vessel permeability changes in otitis media with effusion.
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PMID:Mechanisms of otitis media development. Involvement of neurogenic inflammation. 187 Aug 76

Vascular leakage in the middle ear cavity was studied after i.v. administration of various substances in rats and determined by the Evans blue technique. Bradykinin, histamine, serotonin, acetylcholine, substance P (SP) and vasoactive intestinal polypeptide (VIP) resulted in extravasation of Evans blue. In the case of bradykinin and histamine, the leakage was dose dependent. Calcitonin gene-related peptide (CGRP) did not affect vessel permeability. In other experiments the effect of histamine antagonists was tested on production of middle ear effusion, caused by blowing air at 14 degrees C into the external auditory canal (EAC). The increase in vessel permeability in this otitis media model was inhibited by the H2-receptor antagonist cimetidine, at doses 0.1 and 1.0 mg/ml. Diphenhydramine, an H1-receptor antagonist, arrested only partly middle ear fluid accumulation. Our study demonstrated that various inflammatory mediators and neuropeptides are capable of inducing vascular leakage in the middle ear cavity. It was also concluded that H2-receptors are involved in the regulation of middle ear vascular permeability.
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PMID:Middle ear effusion induced by various inflammatory mediators and neuropeptides. An experimental study in the rat. 247 18

This experiment aimed to explore the effects of substance P (SP) on secretory otitis media (SOM). Both immunohistochemistry ABC-GDN and image pattern analysis technique were adopted to investigate the relation between SP content of SOM middle ear mucosa and middle ear effusion, and observe the effect of SP receptor antagonist spantide and histamine H2 receptor blocker cimetidin on middle ear effusion. The findings showed: middle ear mucosa SP content tended to increase, and had positive correlation with middle ear effusion, intra-abdominally injecting 1 mg/ml Spantide and 1 mg/ml Cinetidin per day could have middle ear effusion decreased obviously, but the quantities of reduction were more significant. The results suggest that SP plays a role in SOM, might accelerate vasodilation and increase the permeability of cupillary in middle ear mucosa mediated by histamine.
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PMID:[The effect of substance P upon middle ear effusion of secretory otitis media and the mode of action]. 981 2

Neurogenic inflammation may play a role in the aetiology of secretory otitis media (SOM). The strongest candidate that initiates the characteristic symptoms of neurogenic inflammation is supposed to be substance P. Capsaicin is a specific antagonist of substance P. The effects of capsaicin on middle ear mucosa have not been studied yet. In an attempt to investigate the effect of pre-treatment with capsaicin on the development of SOM an experimental study was performed. Fourteen Wistar rats were divided into two groups. Seven rats were pre-treated with capsaicin (Group 1) and the others were administered isotonic saline solution (Group 2). Seven days after the third injection rats were operated on and the right tympanal orifice of the Eustachian tube was obstructed. Animals were sacrificed seven days after the operation. Their bullas were excised bilaterally and were studied by light microscopic technique. In Group 1 there was no effusion except for one case. The subepithelial layer was thickened by fibroblast proliferation. Capillary proliferation and some glandular atrophy were observed. In Group 2 the middle ear lumens were filled with effusion. Oedema with dilatation in capillaries and medium-sized vessels of lamina propria was observed as a common feature of the group. Subepithelial fibrosis was found in one case. Capsaicin pre-treatment prevented the formation of effusion in the middle ear lumen in spite of tuba occlusion. The results of this preliminary study lead us to consider that an imbalance in the autonomic innervation of the mucosa of the middle ear may play a role in the aetiology of SOM as in vasomotor rhinitis, and capsaicin may be an alternative in the treatment.
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PMID:Effects of capsaicin pre-treatment in experimentally-induced secretory otitis media. 1039 58