[Effect of CD11b/CD18 on burn-activated PMN-mediated permeability of pulmonary microvascular in isolated perfused lung]

Abstract

Objective: To determine the effect of intercellular adhesion molecule (ICAM-1) CD11b/CD18 in burn-activated PMN-mediated permeability of microvascular in isolated perfused lung.

Method: Isolated lungs were distributed into 7 groups according to the different contents of perfused fluid: normal perfused fluid, normal rat serum, burn rat serum, normal rat PMN, burn rat PMN, normal rat PMN blocked by monoclonal antibody to adhesion molecule CD11b/CD18 and burn rat PMN blocked by antibody. The extent of isolated lung edema, vascular permeability to small molecules (fluid) and vascular permeability to large molecules (albumin) were expressed by lung weight gain (LWG), fluid filtration coefficient (Kf) and pulmonary albumin permeability-surface area product (PS) respectively.

Result: Burn serum could increase LWG, Kf PS, so did burn-activated PMN. The latter could make PS increase more obviously. Monoclonal antibody to CD11b/CD18 on PMN could obviously decrease PMN sequestration in isolated perfused lung. The protective effect of antibody on increasing LWG and Kf, and particularly PS was demonstrated.

Conclusion: (1) The effect of mediators from burn-activated PMN to EC was mediated by PMN adhesion to EC. (2) Some mediators from burn-activated PMN increase mainly the pulmonary vascular permeability to small molecules, and PMN adhesion to EC mediated by CD11b/CD18 may increase directly the permeability to large molecules. (3) Adhesion molecule CD11b/CD18 perhaps have an ability to regulate directly EC by combining its receptor ICAM-1 on EC.