Role of indomethacin-induced peptic ulceration in gastric acid secretion in pregnant rats.
The role of indomethacin-induced peptic ulceration in gastric acid secretion was investigated using albino rats of Wistar strain in early, mid and late pregnancy. The weight ranged between 120 and 180 gm. Non-pregnant rats in estrus served as control. Estrus was induced using the method of Dejalon, Bayo and Dejalon[1] while pregnancy was induced using the method of Bolarinwa and Amure[2,3]. Stomach for perfusion was prepared according to Ghosh[4] with some modification and perfusion was done with 0.15M NaCl solution, using the modified Langerdoff's apparatus. Gastric acid secretion was induced with histamine and carbachol. In general, gastric acid secretion was found to be higher after indomethacin administration than in a control study, and the secretory response was higher to carbachol than to histamine in either case. In rats to which indomethacin had been administered, basal and induced gastric acid secretion was highest in the non-pregnant rats and least in the early-pregnant rats.
Evbuomwan
M I
MI
Department of Physiology, College of Medicine, University of Ibadan, Nigeria.
Bolarinwa
Y
Y
D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D006632:Histamine / Q000494:pharmacology; D007213:Indomethacin / Q000009:adverse effects*; D010437:Peptic Ulcer / Q000139:chemically induced* / Q000503:physiopathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000139:chemically induced* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar
D006632:Histamine; D002217:Carbachol; D007213:Indomethacin