| Abstrakt: |
In dogs with gastric fistulae (GF) and Heidenhain pouches (HP), intravenous graded doses of prostacyclin (PGI2) (dose range: 2.5–20 µg/kg/hr), and prostaglandin E2 (PGE2) (dose range: 10–80 µg/kg/hr) produced a dose-dependent inhibition of acid and pepsin secretion stimulated by pentagastrin (3 µg/kg/hr). The ID50 (dose inhibiting acid output by 50%) were 6 µg/kg/hr for PGI2 and 26 µg/kg/hr for PGE2 for the GF, and 7 µg/kg/hr for PGI2 and 22 µg/kg/hr for PGE2 for the HP. Acid secretion from the GF stimulated by histamine (20 µg/kg/hr) was also inhibited by both prostaglandins: the ID50 were 16 µg/kg/hr for PGI2 and 22 µg/kg/hr for PGE2 For the HP, the ID50 were about 20 and 40 µg/kg/hr for PGI2 and PGE2, respectively. Meal-induced acid secretion from the GF reached a level similar to that observed in tests with pentagastrin and was inhibited by both prostaglandins. The ID50 were 5 and 20 µg/kg/hr for PGI2 and PGE2, respectively. PGI2 significantly increased serum gastrin above that obtained with meal alone whereas PGE2 did not affect postprandial serum gastrin. The inhibition of pentagastrin and meal-induced acid secretion was accompanied by a marked reduction in gastric mucosal blood flow (MBF) measured by the [14C]aminopyrine method, without significant change in the ratio of gastric blood flow to gastric secretion. The MBF in the resting HP mucosa was significantly increased by PGI2 but reduced by PGE2. This study shows that PGI2 is about 3–4 times more potent than PGE2 in inhibiting pentagastrin and meal-induced gastric secretion and MBF; PGI2, unlike PGE2, increases the postprandial serum gastrin and raises the MBF of the resting mucosa. Therefore, both PGI2 and PGE2 are antisecretory, but their effects on gastrin release and resting MBF are qualitatively different. |
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