Experimental and Clinical Studies on Ischemic Lesions of the Large Intestine

• Published in: Nihon Rōnen Igakkai zasshi Vol. 31; no. 11; pp. 835 - 848
• Main Authors: Mizushima, Kazuo, Ashida, Tomohumi, Shibata, Yoshimi
• Format: Journal Article
• Language: Japanese
• Published: Japan The Japan Geriatrics Society 01.11.1994
• Subjects: Adult; Aged; Aortic reconstruction; Arteries; Colitis, Ischemic - etiology; Colitis, Ischemic - pathology; Colon - blood supply; Colon - pathology; Colon ischemia; Colonoscopy; Disease Models, Animal; Dog; Experimental colitis; Female; Humans; Ischemic colitis; Male; Middle Aged; Necrosis
• ISSN: 0300-9173
• DOI: 10.3143/geriatrics.31.835

To clarify the pathogenesis and endoscopic features of ischemic lesions of the colon, experimental ischemia was induced in dogs by arterial ligaiton, gelfoam injection, and clipping. In addition, clinical and endoscopic features of ischemic lesions in ischemic colitis cases in human were studied. In the experimental model, arterial ligation including marginal arteries frequently induced erosions in the large intestine, whereas ligation of the colic artery alone did not induce apparent mucosal lesions of the large intestine. Gelfoam injection to produce thrombi into caudal mesenteric artery or middle colic artery induced ulcers with a high rate of incidence and frequently accompanied by intestinal perforation. Temporal impairment of blood supply by arterial clipping produced erosion, but not ulcers. A high incidence of erosion was obtained in a group that underwent clipping for a prolonged period and a group of recieving Alosenn. Mucosal blood flow measured by the hydrogen gas clearance method was significantly decreased at 1hr and 4hr after gelfoam injection compared with those after arterial ligation. In human cases of ischemia following arterial surgery, endoscopic features were similar to those lesions of the experimental ischemia induced by gelfoam injection. These results suggest that thrombi in peripheral small arteries may play a major role in the pathogenesis of ischemic lesions of the large intestine.