Izole fare mide fundusunda etanole bağli gevşemelerin mekanizmasinin araştirilmasi

Mice (Swiss albino) of either sex were used in this study. After killing the mice by cervical dislocation the gastric fundal strips were prepared by longitudinal incision and mounted under 0.5 g tension in an organ bath filled with Tyrode?s solution. The bath medium was maintained at 37 oC and gassed with %95O2 and 5%CO2. Experimental data were recorded by an isometric transducer.Ethanol caused reproducible relaxations in isolated mouse gastric fundal strips. These relaxations were significantly inhibited by verapamil (10-5,10-4 ,5x10-4 M), a blocker of L-type Ca2+ channel, ruthenium red (10-5, 5x10-5 ,10-4 M), a blocker of ryanodine receptor (intracellular Ca2+ channel), guanethidine (10-6,10-5 ve 10-4 M) a blocker of adrenergic neurons, atropine (10-6, 10-5, 10-4 M), a blocker of cholinergic muscarinic receptors, neomycin (10-5 ,10-4 ,5x10-4 M), an inhibitor of phospholypase C, indomethacin (10-6, 5x10-6,10-5 M), an inhibitor of cyclooxygenase, Nw-nitro-L-arginine (10-5, 10-4 ,5x10-4 M), an inhibitor of nitric oxide synthase and tetraethylammonium (5x10-5, 10-4 ve 5x10-4 M), a blocker of potassium channels. In addition, manoalide (10-6), an inhibitor of phospholypase A2, also inhibited the relaxations induced by ethanol but this inhibition was not significant. However, cyclopiasonic acid (10-6 ,5x10-6 ,10-5 M), a blocker of Ca2+- ATPase and ouabain (10-5, 5x10-5,10-4 M), a blocker of Na+- K+ ATPase and Ca2+- ATPase, failed to affect the relaxations induced by ethanol.The results of experimental data suggest that Ca2+, adrenergic neurons and cholinergic muscarinic receptors, phospholypase C, arashidonic acid-cyclooxygenase patways, nitric oxide and potassium channels play a role on relaxations induced by ethanol. On the other hand, the results also suggest that Ca2+- ATPase and Na+- K+ ATPase did not have a role on relaxations induced by ethanol.Key words: Ethanol, mouse gastric fundus, pharmacological effect, relaxation,