抄録
In order to clarify the angioarchitecture of the esophagus in portal hypertension, barium added gelatin was injected in the esophagus from the left gastric vein in untreated cases and the vascular running was observed macroscopically and histologically. It is classified in three distinct zones as follows; 1. Palisade zone where numerous parallel thin vessels (i. e., the sudare-like veins) run longitudinally, 2. Truncal zone where esophageal varices are commonly formed, 3. Transitional zone where vertically oriented veins run from the palisade zone to the truncal zone. For cases without portal hypertension, many blood vessels were running in lamina propria of the palisade zone. In contrast, for cases with portal hypertension, the corresponding blood vessels were remarkably dilated. The approximate half of them was running in the submucosa, extending the lamina muscularis mucosae. Critical area where esophageal varises frequently rupture corresponds to the transitional zone. A protrusion of a marked piling up of the veins into esophageal lumen and a steeper draining angle of the veins in the critical area are likely to lead to rupture of the varices. Histologically, red color sign corresponds to the thinning of the epithelium due to variceal vein in the lamina propria, and was frequently found in the critical area. The extent of thrombus formation was examined on esophagi of 18 autopsy cases passing more than 2 months after endoscopic injection sclerotherapy (EIS) with 5%ethanolamine oleate. Thrombus formation was observed most extensively in variceal veins in the submucosa of the truncal zone, but was poor in blood vessels of the lamina muscularis mucosa, as was the same with the palisade zone. This suggests that venous dilatation in the lamina muscularis mucosa in mainly responsible for post-EIS relapse.
