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Time-course of development and reversal of gastric endocrine cell hyperplasia after inhibition of acid secretion. Studies with omeprazole and ranitidine in intact and antrectomized rats.
Gastroenterology. 1988 Dec; 95(6):1477-86.G

Abstract

In intact rats plasma gastrin levels were increased during a 20-wk treatment course with either omeprazole or ranitidine. Although plasma gastrin levels were the same during treatment, the enterochromaffinlike (ECL) cell density increased approximately linearly with time at a rate correlated to the plasma gastrin level. Antrectomy prevented the ECL cell hyperplasia seen in omeprazole-treated rats, suggesting that it was not caused by omeprazole per se. Changes in ECL cell density roughly paralleled changes in oxyntic mucosal histidine carboxylase activity and histamine concentration. Treatment with omeprazole also raised stomach weight and antral gastrin and gastrin cell density, reduced antral somatostatin cell density, but did not affect enterochromaffin cell density. Within 19 days of cessation of a 10-wk treatment course, plasma gastrin levels, oxyntic mucosal histidine decarboxylase activity, and antral gastrin and somatostatin cell densities had returned to control levels. The stomach weight was normal within 5-10 wk, antral gastrin concentration within 10 wk, and oxyntic mucosal ECL cell density and histamine concentration within 20 wk. After renewed treatment with omeprazole for 10 wk starting 10 wk after completion of the first omeprazole treatment period, changes in all parameters were of similar magnitude in animals previously treated with omeprazole and those previously treated with vehicle. The results suggest that the effects described are reversible and that gastrin cells turn over more rapidly than ECL cells.

Authors+Show Affiliations

Department of Biology, AB Hässle, Mölndal, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

3181674

Citation

Larsson, H, et al. "Time-course of Development and Reversal of Gastric Endocrine Cell Hyperplasia After Inhibition of Acid Secretion. Studies With Omeprazole and Ranitidine in Intact and Antrectomized Rats." Gastroenterology, vol. 95, no. 6, 1988, pp. 1477-86.
Larsson H, Carlsson E, Håkanson R, et al. Time-course of development and reversal of gastric endocrine cell hyperplasia after inhibition of acid secretion. Studies with omeprazole and ranitidine in intact and antrectomized rats. Gastroenterology. 1988;95(6):1477-86.
Larsson, H., Carlsson, E., Håkanson, R., Mattsson, H., Nilsson, G., Seensalu, R., Wallmark, B., & Sundler, F. (1988). Time-course of development and reversal of gastric endocrine cell hyperplasia after inhibition of acid secretion. Studies with omeprazole and ranitidine in intact and antrectomized rats. Gastroenterology, 95(6), 1477-86.
Larsson H, et al. Time-course of Development and Reversal of Gastric Endocrine Cell Hyperplasia After Inhibition of Acid Secretion. Studies With Omeprazole and Ranitidine in Intact and Antrectomized Rats. Gastroenterology. 1988;95(6):1477-86. PubMed PMID: 3181674.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Time-course of development and reversal of gastric endocrine cell hyperplasia after inhibition of acid secretion. Studies with omeprazole and ranitidine in intact and antrectomized rats. AU - Larsson,H, AU - Carlsson,E, AU - Håkanson,R, AU - Mattsson,H, AU - Nilsson,G, AU - Seensalu,R, AU - Wallmark,B, AU - Sundler,F, PY - 1988/12/1/pubmed PY - 1988/12/1/medline PY - 1988/12/1/entrez SP - 1477 EP - 86 JF - Gastroenterology JO - Gastroenterology VL - 95 IS - 6 N2 - In intact rats plasma gastrin levels were increased during a 20-wk treatment course with either omeprazole or ranitidine. Although plasma gastrin levels were the same during treatment, the enterochromaffinlike (ECL) cell density increased approximately linearly with time at a rate correlated to the plasma gastrin level. Antrectomy prevented the ECL cell hyperplasia seen in omeprazole-treated rats, suggesting that it was not caused by omeprazole per se. Changes in ECL cell density roughly paralleled changes in oxyntic mucosal histidine carboxylase activity and histamine concentration. Treatment with omeprazole also raised stomach weight and antral gastrin and gastrin cell density, reduced antral somatostatin cell density, but did not affect enterochromaffin cell density. Within 19 days of cessation of a 10-wk treatment course, plasma gastrin levels, oxyntic mucosal histidine decarboxylase activity, and antral gastrin and somatostatin cell densities had returned to control levels. The stomach weight was normal within 5-10 wk, antral gastrin concentration within 10 wk, and oxyntic mucosal ECL cell density and histamine concentration within 20 wk. After renewed treatment with omeprazole for 10 wk starting 10 wk after completion of the first omeprazole treatment period, changes in all parameters were of similar magnitude in animals previously treated with omeprazole and those previously treated with vehicle. The results suggest that the effects described are reversible and that gastrin cells turn over more rapidly than ECL cells. SN - 0016-5085 UR - https://www.unboundmedicine.com/medline/citation/3181674/Time_course_of_development_and_reversal_of_gastric_endocrine_cell_hyperplasia_after_inhibition_of_acid_secretion__Studies_with_omeprazole_and_ranitidine_in_intact_and_antrectomized_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016-5085(88)80066-0 DB - PRIME DP - Unbound Medicine ER -