1992 Volume 34 Issue 11 Pages 2565-2575
Acute gastric mucosal lesions associated with hepatic arterial embolization have been reported to arise chiefly from the backflow of embolic materials into the gastric arteries. We performed a basic study using mongrel dogs to clarify whether the incidence, morphology, and mechanism of onset of these lesions varied with different embolic substances. Various substances were infused into 5 groups of dogs via a gastroepiploic arterial catheter inserted by the Seldinger method. In the Lipiodol group, the gastric mucosal blood flow was reduced transiently and redness developed in 17% (1/6), but no ulcers were observed. In the mitomycin-C (MMC) group, the gastric mucosal blood flow did not decrease. Erythema occurred in 3 out of 5 dogs (60%), apparently due to some cause other than ischemia. In the Lipiodol-MMC group, gastric mucosal ischemia was prolonged and the incidence of ulcers was high (57%, 4/7). Synergy between ischemia due to long period retention of the suspension in the gastric mucosa and the cytopathic effect of MMC appeared to produce this result. Gelfoam powder induced a prolonged reduction in gastric mucosal blood flow as did the Lipiodol-MMC suspension, and caused a high incidence of ulcers apparently due to ischemia (100%, 6/6). In the Gelf oam tips (1×1mm) group, the reduction in gastric mucosal blood flow was transient as with Lipiodol alone, but erosions and erythema were observed (50%, 2/4). Preventive treatment with a prostaglandin E1 derivative increased gastric mucosal blood flow (137.2%), and reduced the incidence of ischemic mucosal lesions when compared with the control group (100%→50%).
