RESUMO
AIM:To establish an experimental model of stress ulcer produced by explosive noise, and to probe into its mechanism and protection.METHODS:The country standard Wistar white rats were randomly divided into control group(n =8), which were neither stimulated nor protected, and stimulating group (divided into subgroups A, B and C, including 8 rats each which were decapitated to draw blood for test immediately, 12 hours and 24 hours after stimulation) and prevention group (divided into subgroups A, B and C, having 8 rats each, subgroup A was given cimetidine, B anisodamine and C both drugs). Firing noises of submachine guns were used as inflicting factor. The rats were fasted for 24 hours and stimulated by firing noise for 12 hours. The change of ulcer index, gastric mucosal and related serum hormones were observed.RESULTS:Stress ulcer was significant in the stimulating group, and its ulcer index (8.6 ± 0.6) was remarkably higher than that in both the control group and prevention group (0.3 ± 0.1, P < 0.01).Its serum gastrin (Gas ng/L, 294 ± 163 vs 63 ± 40,P< 0.01) and endothelin (ET ng/L, 181 ± 57 vs 135 ± 42, P < 0.1) were apparently higher than those in the control group, and its serum nitric oxide (NO) level was conspicuously lower than that in the control group (ng/L, 0.3 ± 0.1 vs 0.8 ± 0.5 P <0.5), while the serum gastrin level (ng/L, 556 ± 225) in prevention group was distinctly higher than that in both the control (P<0.1) and stimulating group (P < 0.5). There were no significant differences in the changes of ET and NO between the control and the stimulating groups.CONCLUSION:Stress ulcer model of rats can be successfully established by the stimulation of explosive noise. Gas, ET and NO are related to the formation of stress ulcer, and play an important role in its mechanism. Hepatic function affected by noise is observed in this experiment.