Kusche J, Stahlknecht C D, Lorenz W, Reichert G, Richter H
Agents Actions. 1977 Mar;7(1):81-4. doi: 10.1007/BF01964885.
Following superior mesenteric artery occlusion and revascularization in dogs all animals died in a circulatory collapse state. However, pretreatment by aminoguanidine, the strong and specific inhibitor of diamine oxidase, accelerated the circulatory break-down significantly and increased the venous plasma histamine concentrattions up to levels which also in normal dogs are effective in the circulatory system. Furthermore, the haematocrit increased significantly more in the aminoguanidine-treated animals than in the dogs treated by saline. No changes in plasma diamine oxidase activity were observed in saline-treated animals during intestinal ischemia and following revascularization. In aminoguanidine-treated animals no enzymic activity could be measured. The results were interpreted by a protective role of intestinal diamine oxidase in intestinal ischemia. Enhancement of the enzymic activity in patients, for instance by heparin, may be helpful in mesenteric infarction disease.
在犬肠系膜上动脉闭塞和血管再通后,所有动物均死于循环衰竭状态。然而,用二胺氧化酶的强效特异性抑制剂氨基胍进行预处理,显著加速了循环崩溃,并使静脉血浆组胺浓度升高至在正常犬中对循环系统也有效的水平。此外,与用生理盐水处理的犬相比,氨基胍处理的动物的血细胞比容显著升高。在用生理盐水处理的动物中,在肠缺血期间和血管再通后未观察到血浆二胺氧化酶活性的变化。在氨基胍处理的动物中无法检测到酶活性。这些结果被解释为肠二胺氧化酶在肠缺血中具有保护作用。例如,通过肝素增强患者的酶活性可能有助于治疗肠系膜梗死疾病。