Do leukocyte adhesion molecules mediate renal reperfusion injury?
With evidence implicating leukocytes and oxygen free-radicals in renal reperfusion injury, there has been recent interest in delineating the role of leukocyte adhesion molecules in these processes. In animal experiments administration of monoclonal antibodies to leukocyte adhesion molecules has attenuated reperfusion damage in many organs, including heart, liver and skeletal muscle (14, 48). As compared to control rats, administration of blocking monoclonal antibodies to the CD11a & CD11b subunits prior to 60 min of renal artery occlusion was associated with a 25% lower serum creatinine and less evidence of pathologic damage 24 hours later (9). Although the increase in renal neutrophils was slightly lower in the treatment group, it was not statistically significant (9). These same antibodies virtually abolished neutrophil migration to LPS-stimulated dermis (9), but caused little change in airway leukocytes while significantly attenuated allergic airway hyperresponsiveness to antigen (4
