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

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