Inhibition of HCl secretion and the effects on ultrastructure and electrical resistance in isolated piglet gastric mucosa.
Rates of H+ secretion and transepithelial resistance were measured for gastric mucosas from neonatal piglets before and after the addition of histamine and with the deployment of conditions that inhibit HCl secretion. At designated times tissue biopsy specimens were taken and prepared for electron microscopy. Oxyntic cell morphology was evaluated by classification of the cells into one of four categories: resting, partially stimulated, stimulated, or returning. Morphologic profiles for each experimental condition were thus established. In order to assess this method of quantitation, detailed morphometric analyses of oxyntic cells from resting and stimulated preparations were undertaken. The observed differences in tubulovesicular and microvillar surface densities were similar to those of previous investigators and correlated well with the morphologic profiles for these conditions. Actively secreting gastric preparations subjected to 15 mM NaSCN, substrate deprivation, or removal of histamine showed an inhibition of HCl secretion coupled with an increase in tissue resistance. However, only the morphologic profile of cells from the latter condition was different from that observed for control stimulated cells; histamine removal caused cells to be predominantly of a resting or returning morphology. Treatment of resting tissue with SCN- or removal of substrate inhibited subsequent histamine-induced secretion though tissue resistance decreased somewhat (approximately 15%). The morphologic profile of cells from these conditions was similar to that of control stimulated cells, despite the lack of acid secretion. These data support the hypothesis that oxyntic cell morphology does not absolutely dictate the secretory state of the tissue and that the resistance of gastric mucosa cannot be accounted for solely by the ultrastructure (i.e., surface area) of oxyntic cells.
D000818:Animals; D004594:Electrophysiology; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D013552:Swine