Mechanism of stress ulcer - analysis from the viewpoint of neuro-endocrine-immune system.

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Acute food restriction has been thought to induce psychosomatic stress in man and has been shown to develop stress ulcers in murine stomach. Recently, increasing evidence has been found which suggests that stress hormones, some lymphokines and neuropeptidesmay represent an information channel in the neuro-endocrine-immune system in stress. In the present study we imposed food restriction on young adult, C3H/He mice, for 1-5 days and studied the serial changes of various immune parameters, together with the endogenous level of some stressassociated humoral factors to clarify their implications in acute food restriction. Daily 23-h food deprivation for 1-5 days induced gastric ulcers and atrophic changes of the splean and thymus, accompanied by a rise inplasma cortisol and catecholamine levels in mice. It also modulated several immune cell functions in the splean including a drop in the B cell population but no change in the mitogen response of the B cells, an increase in T cell population but no change in the L3T4/Lyt 2 ratio and an early increase in natural killer activity and O_2^- production by macrophages. These effects are thought to correlate to the increase in stress-associated humoral factors and this may partly result from stress induced by food restriction. Recently, free radical-mediated injury of gastric mucosa has been suggested to be involved in some sort of stress. We studied the activities of antioxidant enzymes in gastric mucosa to clarify the role of free radicals in stress-induced response. Among the enzyme activities, only SOD activity was decreased before the development of acute gastric mucosal lesion. The laws of the activity may play some role in the progress of AGNL.