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 interrelationship between somatostatin and its synthetic analog, sandostatin, with neuropeptides and inflammatory mediators, as well as their protection of gastric mucosal damage, were tested in rats. Rats were treated intragastrically with 1.0 ml of 96% ethanol with or without intravenous or intraperitoneal coadministration of somatostatin (1.0 microM/kg). Mucosal damage was also induced by the administration of either indomethacin (30 mg/kg subcutaneously) with or without intravenous sandostatin (10 micrograms/rat), given 30 min prior to damage induction. Somatostatin levels in ethanol-damaged gastric mucosa were significantly lower than in control rats. Substance P and vasoactive intestinal peptide (VIP) levels were significantly higher in the damaged mucosa in rats treated with ethanol, as was the mucosal generation of leukotriene B4 (LTB4) and cysteinyl-containing leukotrienes. The coadministration of somatostatin with ethanol significantly reduced gastric mucosal injury induced by ethanol alone. The protection of the mucosa was accompanied by reduction of mucosal substance P and VIP levels, as well as the generation of leukotrienes, an effect that was reversed by intraperitoneal or intravenous coadministration of somatostatin antagonist, cyclo-(7-aminoheptanoyl-PH-E-D-Trp-Lys-THR), 1.0 microM/100 g, with somatostatin (1.0 microM/kg) and ethanol. When given by itself somatostatin significantly reduced mucosal leukotriene generation compared with their generation in saline-treated rats. Sandostatin completely abolished gastric mucosal damage induced by indomethacin administration. In rats treated with somatostatin and indomethacin, this effect was accompanied by reduction of mucosal leukotriene generation. Administration of sandostatin to pylorus-ligated rats significantly reduced gastric acid output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatostatin effectively prevents ethanol- and NSAID-induced gastric mucosal damage in rats. 751 Jun 7

A case of carcinoid tumour of the small intestine has been reported, which caused hormone producing multiple hepatic metastases. The 45 year old man had flush syndrome several times a day, that was caused by a carcinoid tumour originated from the jejunum. After the operation of the primary tumour he was treated by Sandostatin (Sandoz, Basel), which significantly reduced the symptoms and slowed down the progression. The neural elements containing substance P, neuropeptide Y, vasoactive intestinal polypeptide, serotonin, dopamine-beta-hydroxylase and somatostatin, which are thought to cause the symptoms, were investigated in the small intestine and the liver metastasis by an immunocytochemical method. It seems to be an interesting observation, that a large number of neuropeptide Y immunoreactive nerve fibers and some substance P and vasoactive intestinal polypeptide immunoreactive nerve processes and cell bodies were observed however, no trace of somatostatin and serotonin immunoreactive nerve elements could be detected in the hepatic metastasis. That can be a novel addition to the possible aetiology of the carcinoid syndrome and to the way how the somatostatin treatment acts.
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PMID:[Treatment of carcinoid tumor with a long-acting somatostatin analog]. 843 17