Haglund U
Acta Chir Scand Suppl. 1985;526:66-72.
Experimental animals develop a characteristic mucosal damage in the small intestine following shock and hypotension. Similar lesions have also been described in man. The damage is caused by hypoxia and, in addition, proteolytic activities and generation of oxygen derived free radicals may be important. The small intestinal mucosal damage is associated with the development of cardiovascular collapse--hypotension induces mucosal lesions which, in turn aggravate the lesions. Among proposed mechanisms are portal invasion of bacteria and release of cardiotoxic material to the venous blood. Methylprednisolone in high doses (30 mg/kg) has been demonstrated to prevent or delay the development of mucosal lesions. This is probably not due to cardiovascular effects but rather to a stabilizing effect on cellular and subcellular membranes.
实验动物在休克和低血压后,小肠会出现特征性的黏膜损伤。人类也有类似病变的描述。这种损伤是由缺氧引起的,此外,蛋白水解活性和氧衍生自由基的产生可能也很重要。小肠黏膜损伤与心血管衰竭的发生有关——低血压会诱发黏膜病变,进而加重损伤。提出的机制包括细菌的门静脉入侵和心脏毒性物质释放到静脉血中。高剂量(30毫克/千克)的甲基强的松龙已被证明可预防或延缓黏膜病变的发生。这可能不是由于心血管效应,而是对细胞膜和亚细胞膜具有稳定作用。