Abstract
Summary
Experiment 1 demonstrated that gastric mucosal damage in rats induced by lateral hypothalamic (LH) lesions could be significantly reduced by antisecretory doses of propantheline, cimetidine, and by vagotomy, however, only propantheline also prevented hypersalivation and chromodacryorrhea. These results indicate that a primary effect of LH lesions is to produce an abrupt increase in parasym-pathetic activity. Experiment 2 showed that gastric mucosal barrier functions were altered by LH lesions even before visible defects of the mucosa were present. It is suggested that an increase in permeability of the gastric mucosa may play an important role in the pathogenesis of gastric ulceration induced by hypothalamic damage.
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