Abstract
The gastric microvascular changes in reserpine (RES 6 mg/kg s.c.)-induced ulcer in Wistar male rats were studied. Two kinds of water paints were injected through the superior mesenteric vein and celiac artery. Excised stomachs were frozen instantly by cooled methanol (-70°C) and were put into methylsalicylate after 24 hr in order to make transparent preparations. RES caused constriction of the vein from the middle layer till the muscularis mucosae and congestion with ischemia in the gastric mucosa after 1 hr. Even after 3 hr, these vascular changes remained and were accompanied by erosion. After 6 and 9 hr, the erosion became more severe, while ischemia was no longer found and the vessels were rather dilated. These lesions initiated from the fundic-antral border area in the lesser curvature and gradually extended to the greater curvature. The early changes up to 3 hr were inhibited by phentolamine, isoproterenol, C6, metiamide and methysergide, but not by carbachol, atropine, vagotomy and propranolol. Atropine, vagotomy, isoproterenol, propranolol and C6 inhibited erosion in the late stage. Phentolamine, carbachol, diphenhydramine, metiamide and methysergide were not effective. From these results and the gastric movement caused by RES, it is suggested that the vascular changes of the early stage in RES-induced ulcer are due not only to the autonomic nervous system but also to the endogenous biogenic amines, and the erosions in the late stage depend on the hypermotility of the stomach rather than on the hypersecretion of the stomach.
