| pubmed-article:43586 | pubmed:abstractText | Six 20- to 25-year-old healthy men were studied with an intravenous pentagastrin infusion in a dose of 6 micrograms/kg-h for 4.5 h. Four of these were also studied on separate days with an intravenous secretin infusion in a dose of 2 CU/kg-h for 4.5 h. Gastric juice was collected continuously for one 30-min period before and in 30-min periods throughout the infusion periods, and the gastric H+ and pepsin outputs were determined during the pentagastrin infusion only. Blood was drawn before, every 30 min throughout the infusion, and the next morning for determination of serum group I pepsinogens (PG I), serum gastrin, and plasma secretin. Pentagastrin evoked a sustained rise in gastric H+ and pepsin secretions, a more delayed and sustained increase in serum PG I in the four subjects with a normal pentagastrin-stimulated maximal gastric secretion, and a fall in serum PG I in the remaining two subjects with a low gastric secretion. Secretin also elicited a sustained elevation in serum PG I in all four examined, including one who showed a fall in serum PG I during pentagastrin infusion. It is proposed that pentagastrin may exert its stimulatory effect of pepsinogen synthesis subsequent to degranulation of the chief cells, whereas secretin may stimulate the pepsinogen synthesis more directly. Thus, the fall in serum PG I during pentagastrin infusion in the two subjects with low gastric secretion may possibly be due to a defective cellular storage of PG I in atrophic gastritis. Plasma secretin was not affected by gastric suction or by prolonged infusion of pentagastrin, whereas serum gastrin fell during secretion infusion accompanied by gastric suction. | lld:pubmed |
