High doses of corticosteroids in the prevention of small intestinal mucosal damage in shock.
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.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D007410:Intestinal Diseases / Q000209:etiology / Q000517:prevention & control; D007413:Intestinal Mucosa / Q000098:blood supply / Q000473:pathology; D007421:Intestine, Small / Q000098:blood supply / Q000473:pathology*; D008775:Methylprednisolone / Q000627:therapeutic use; D012769:Shock / Q000150:complications* / Q000188:drug therapy; D012771:Shock, Hemorrhagic / Q000150:complications / Q000188:drug therapy; D012772:Shock, Septic / Q000150:complications / Q000188:drug therapy
D000305:Adrenal Cortex Hormones; D008775:Methylprednisolone