Gl. Eastwood et al., NICOTINE HAS NO EFFECT ON RAT GASTRIC-MUCOSAL PROSTAGLANDIN GENERATION IN-VITRO, Digestive diseases and sciences, 38(8), 1993, pp. 1450-1452
Previous studies have shown that cigarette smoking depresses prostagla
ndin generation by human gastric mucosa, but the component of smoke th
at is responsible for that action is not known. To investigate whether
nicotine has a direct effect on gastric mucosal prostaglandin generat
ion, we performed the following study. Eight rats were sacrificed and
the stomachs removed. Using a biopsy forceps, small pieces of gastric
mucosa were resected and placed in incubation vials containing either
buffered Krebs solution alone (control), Krebs solution plus indometha
cin (5 mug/ml), or Krebs solution plus one of several concentrations o
f nicotine ditartrate (10, 100, 500, 1000 ng/ml). The nicotine concent
rations we used ranged below and above the plasma nicotine concentrati
ons of smokers shortly after smoking cigarettes. Three separate incuba
tions of gastric mucosa were performed per experimental group from eac
h animal. After 30 min of incubation, prostaglandin E2 and 6-keto-pros
taglandin F1alpha concentrations in the incubation medium were measure
d by radioimmunoassay. We found that nicotine at any concentration tes
ted had no effect on the generation of prostaglandin E2 and 6-keto-pro
staglandin F1alpha by rat gastric mucosa. Thus, this study indicates t
hat, if nicotine is involved in the depression of prostaglandin genera
tion in the gastric mucosa of smokers, its role is an indirect one and
not by direct action on the gastric mucosa.