The role of melatonin and nitric oxde in the response of rat fundusstrips to electrical field stimulation in A peptic ulcer model

The aim of the study is to investigate the role of melatonin(MLT) and nitric oxide (NO) on electrical field stimulation(EFS) responses in peptic ulcer model. Experimental groups were established as (1) Control, (2) Ulcer (60% ethanol, 5ml/kg oral), (3) in-vivo Melatonin (15mg/kg, ip, 30 minutes before sacrificing), (4) Melatonin+Ulcer (15mg/kg, ip melatonin 30 minutes before ulcer). The effects of L-NAME (NOS-inhibitor), DEA-NO (NO-Donor) and in-vitro melatonin on EFS (40V,8Hz)-mediated contractile responses in the presence of guanethidine and indomethacin in rat stomach fundus strips were investigated. Carbachol responses were recorded in all experimental groups to evaluate exogenous cholinergic responses.The ulcer area was measured as millimeters. Data were calculated as mean SE.Kruskal-Wallis, Friedman, Mann Whitney U, Wilcoxon tests were used for statistics. The ulcer score was 11.52 6.12 0.54 mm in melatonin+ulcer group;the difference was significant. EFS responses decreased significantly in ulcer group and there was no difference in KCL responses. There was no improvement in these responses in the melatonin+ulcer group.L-NAME increased EFS responses in all groups; no significant difference was found between the groups DEA-NO and in-vitro melatonin decreased EFS responses in a concentration-dependent manner in control and ulcer groups. Reducing effect of DEA-NO on EFS responses was higher in the control than the ulcer group.When responses created by melatonin in a concentration-dependent manner evaluated on EFS-mediated contraction responses in the presence of L-NAME, it was found that these responses were decreased in both control and ulcer groups, but there was no statistical difference.Contractile responses caused by Carbachol were significantly decreased in ulcer group, and this decrease tended to turn back to normal in the in-vivo melatonin groups. Melatonin reduced ulcer formation. Ulceration disrupts the neurogenic contractions triggered by EFS in fundus, and in-vivo melatonin does not provide improvement on it. Decreased effects of NO donor and carbachol responses in ulcerated tissue suggest that the damage is postsynaptic. Key Words: Peptic ulcer, melatonin, electrical field stimulation, nitric oxide