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Search: WFRF:(Mattsson H.) > (1995-1999) > Gastric acid secret...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003167naa a2200277 4500
001oai:lup.lub.lu.se:c0fc5776-0f2c-4336-8ad7-0030eef8d96b
003SwePub
008160404s1996 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/301812 URI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Andersson, K4 aut
2451 0a Gastric acid secretion after depletion of enterochromaffin-like cell histamine. A study with a-fluoromethylhistidine in rats
264 1c 1996
520 a BACKGROUND: Histamine is thought to play a central role in the regulation of gastric acid secretion. In the rat oxyntic mucosa most of the histamine is synthesized and stored in enterochromaffin-like (ECL) cells, and the rest resides in mast cells. The present study examines the role of ECL-cell histamine in the control of acid secretion in the intact, conscious rat. METHODS: Rats were treated with alpha-fluoromethylhistidine (alpha-FMH) to inhibit histamine synthesis. alpha-FMH was given by continuous subcutaneous infusion (3 mg/kg/h) for up to 9 days. An additional oral dose of alpha-FMH (50 mg/kg) was given 2 h before each acid secretion test. Acid secretion was studied in pylorus-ligated rats and in chronic gastric fistula rats stimulated with histamine, gastrin-17, or insulin after 2-6 days of alpha-FMH infusion. RESULTS: Treatment with alpha-FMH lowered oxyntic mucosal histamine synthesis by 80%. From previous observations this is thought to reflect depletion of histamine from the ECL cells. The remaining 20% resides in mucosal and submucosal mast cells, which seem to be resistant to alpha-FMH. Basal acid secretion was inhibited by more than 60% after alpha-FMH treatment and by more than 80% by ranitidine. Histamine-stimulated secretion was unaffected by alpha-FMH and abolished by the histamine H2-receptor antagonist ranitidine. The acid response to gastrin-17 was almost abolished in histamine-depleted rats and abolished by ranitidine. Vagally induced acid secretion (provoked by the injection of insulin or by pylorus ligation) was unaffected by alpha-FMH treatment but abolished by ranitidine and by the muscarinic M1-receptor antagonist pirenzepine. CONCLUSION: The results suggest that gastrin stimulates acid secretion by releasing histamine from ECL cells. Vagally induced acid secretion is also dependent on a histaminergic pathway but not on ECL-cell histamine.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng
700a Cabero, J L4 aut
700a Mattsson, H4 aut
700a Håkanson, Rolfu Lund University,Lunds universitet,Drug Target Discovery,Forskargrupper vid Lunds universitet,Lund University Research Groups4 aut0 (Swepub:lu)farm-rha
710a Drug Target Discoveryb Forskargrupper vid Lunds universitet4 org
773t Scandinavian Journal of Gastroenterologyg 31:1, s. 24-30q 31:1<24-30x 1502-7708
8564 8u https://lup.lub.lu.se/record/30181

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Andersson, K
Cabero, J L
Mattsson, H
Håkanson, Rolf
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MEDICAL AND HEALTH SCIENCES
MEDICAL AND HEAL ...
and Basic Medicine
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Scandinavian Jou ...
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Lund University

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