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Titolo:
THE ENTEROCHROMAFFIN-LIKE (ECL) CELL - PHYSIOLOGICAL AND PATHOPHYSIOLOGICAL ROLE
Autore:
WALDUM HL; SANDVIK AK; SYVERSEN U; BRENNA E;
Indirizzi:
UNIV HOSP TRONDHEIM,DEPT MED N-7006 TRONDHEIM NORWAY UNIV TRONDHEIM,INST CANC RES TRONDHEIM NORWAY
Titolo Testata:
Acta oncologica
fascicolo: 2, volume: 32, anno: 1993,
pagine: 141 - 147
SICI:
0284-186X(1993)32:2<141:TE(C-P>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERFUSED RAT STOMACH; ZOLLINGER-ELLISON SYNDROME; CHRONIC ATROPHIC GASTRITIS; STIMULATED ACID-SECRETION; CANINE PARIETAL-CELLS; ENDOCRINE-CELLS; HISTAMINE-RELEASE; OXYNTIC MUCOSA; FUNDIC MUCOSA; CARCINOID-TUMORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
110
Recensione:
Indirizzi per estratti:
Citazione:
H.L. Waldum et al., "THE ENTEROCHROMAFFIN-LIKE (ECL) CELL - PHYSIOLOGICAL AND PATHOPHYSIOLOGICAL ROLE", Acta oncologica, 32(2), 1993, pp. 141-147

Abstract

Histamine has a central role in the regulation of gastric acid secretion. This histamine is produced by and released from the enterochromaffin-like (ECL) cell which accordingly has a key-regulatory role in theoxyntic mucosa. Gastrin and the vagal nerves stimulate the formation and release of histamine from the ECL cell. Moreover, gastrin and the vagal nerves also stimulate the proliferation of the ECL cell. An increased ECL cell density may partly explain the increased acid secretionin patients with duodenal ulcer, particularly in patients with Zollinger-Ellison syndrome. The reduced potency of histamine-2 blockers in patients with Zollinger-Ellison syndrome is probably due to increased histamine release by an elevated ECL cell mass. Prolonged and profound hypergastrinemia may lead to ECLomas. Moreover, a proportion of diffuse gastric carcinomas may originate from ECL cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:33:52