Lower Body Ischemia-Reperfusion during
Ischemia and reperfusion result in leukocyte activation, adhesion and infiltration, which can extend tissue injury in experimental stroke and myocardial infarction. Activated neutrophils are considered the primary mediators of tissue destruction following ischemia and reperfusion. This involves adhesion to the endothelial surface and tissue infiltration, followed by eventual release of toxic reactive oxygen metabolites and proteases by neutrophils. The activation of neutrophils and monocytes is accompanied by an increase in cell-surface density of the adhesion molecules CD1 lb and CD 18, which play an important role in leukocyte adhesion and infiltration. The critical role of these adhesion molecules is clearly demonstrated by the observations that inhibition of leukocyte adhesion with antibodies directed against CD 18 or the CD18/CD11 dimers can reduce the extent of injury.
Surgical repair of abdominal aortic aneurysm involves extended clamping and declamping of the aorta, which necessarily results in ischemia and reperfusion of the lower half of the body. Given the large volume of the affected tissues and the unimpeded venous return from the ischemic sites following restoration of blood flow, we hypothesized that this surgical procedure would result in marked upregulation of leukocyte integrins in the systemic circulation. To test this hypothesis, we measured neutrophil and monocyte surface densities of CD1 lb and CD 18 in serial blood samples obtained from radial artery (representing systemic blood) and femoral vein (representing blood draining the ischemic tissues) in a group of patients undergoing elective abdominal aortic aneurysm repair. cheap levitra online
Tags: adhesion molecules, CD1 lb/CD 18, inflammation, leukocytes, vascular endothelium