Gastrin (g) and enterochromaffin: Like (ecl) cells in the stomach of portocaval-shunted rats: Radioimmunological, immunocytochemical and ultrastructural study

Radosavljevic Tatjana, Todorovoc Vera, Nikolic Ivan, Petakov Marijana, Sikic Branka, Vucevic Danijela
2005 Acta Veterinaria  
The aim of the study was to monitor the changes observed in the concentration of gastrin, as well as the morphological and ultrastructural properties of pyloric G and fundic ECL cells in rats with a portocaval shunt (PCS). Eight weeks after surgery, plasma and pyloric tissue gastrin concentrations were determined by radioimmunoassay. Sections from pyloric mucosa were immunostained for the identification of G cells, while oxyntic mucosa specimens were processed for Sevier-Munger detection of ECL
more » ... er detection of ECL cells. In addition, ultrastructural properties of G and ECL cells were determined by standard transmission electron microscopy. The results showed that the plasma gastrin levels were unchanged, while the pyloric gastrin concentrations were significantly increased in rats with PCS compared to the control animals (p<0.01). The morphometric analysis showed a significant increase in the cell density of antral G cells (p<0.05) and fundic ECL cells (p<0.01), as well as an increased number of these cells per mm 2 of mucosa (p<0.01). In addition, the ECL cell profile area was increased in rats with PCS. The predominance of very large vesicles and the reduction of normal cytoplasmic granules and vesicles was a prominent subcellular feature of the ECL. G-cells in PCS rats showed the presence of secretory granules of all types (electron-dense, electron-lucent and electron-pale). The number of electron dense granules was elevated. These ultrastructural patterns are compatible with the functional activation of G and ECL cells. The present study suggests that PCS results in hyperplasia of G cells, as well as in both hyperplasia and hypertrophia of ECL cells. It is highly probable that the PCS enchances the sensitivity of the ECL cells to gastrin, thereby enabling them to respond to gastrin in an exaggerated manner.
doi:10.2298/avb0501023r fatcat:jkctdgcf3rea7nqdkartjhstki