Abstract The advent of celiac angiography has verified the fact that variations in the origin of the larger arteries to the stomach are frequent and need to be considerd in gastric surgery. The submucosal plexus of the fundus and body of the stomach differs markedly from that of the lesser curvature, pyloric region, and proximal part of the first portion of the duodenum. In the former area, the anastomotic network is extremely rich, at times being spongelike in character. In the latter, it is sparse, anastomoses are longer and farther apart, and the mucosal arteries have their origin frequently external to the muscularis propria, making mucosal circulation at times precarious. In the body and fundus, structural abnormalities in the submucosal plexus only a millimeter or two in diameter are frequently seen and may present themselves as angiomas, chaotic vascular abnormalities, and arterial degeneration. Although proof is not finite, it is suggested that these abnormalities result from turbulence at the site of direct, uncompensated arterial anastomoses. The overlying mucosa is often atrophic and may become necrotic with ensuing hemorrhage. When the sphincters of the arteriovenous fistulas become decompensated, as is often the case in cirrhosis, the venous limbs in the lower esophagus, fundus, and body, where they are normally present, lacking adequate external support to control the increase in intramural pressure, dilate, and form huge varices. It is probable that mucosal perfusion in the stomach is phasic with gastric function. That the relative ischemia of the lesser curvature, pyloric area, and upper part of the first duodenum may be the cause of peptic ulcer is difficult to justify. In all probability, however, it does play a part, particularly in determining the site of the ulcer and contributing to its chronicity.