Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Mechanisms of leukocyte distribution during sepsis: an experimental study on the interdependence of cell activation, shear stress and endothelial injury. | Ploppa et al. Critical Care 2010 14 R201 http content 14 6 R201 c CRITICAL CARE RESEARCH Open Access Mechanisms of leukocyte distribution during sepsis an experimental study on the interdependence of cell activation shear stress and endothelial injury 1 1 2 1 11 Annette Ploppa Volker Schmidt Andreas Hientz Joerg Reutershan Helene A Haeberle Boris Nohé Abstract Introduction This study was carried out to determine whether interactions of cell activation shear stress and platelets at sites of endothelial injury explain the paradoxical maldistribution of activated leukocytes during sepsis away from local sites of infection towards disseminated leukocyte accumulation at remote sites. Methods Human umbilical venous endothelial cells HUVEC and polymorphonuclear neutrophils PMN were activated with lipopolysaccharide at 100 and 10 ng ml to achieve adhesion molecule patterns as have been reported from the hyper- and hypo-inflammatory stage of sepsis. To examine effects of leukocyte activation on leukocyte-endothelial interactions activated HUVEC were perfused with activated and non-activated neutrophils in a parallel plate flow chamber. Adhesion molecule expression and function were assessed by flow cytometry and blocking antibodies. In a subset of experiments the sub-endothelial matrix was exposed and covered with platelets to account for the effects of endothelial injury. To investigate interactions of these effects with flow all experiments were done at various shear stress levels 3 to dyne cm2 . Leukocyte-endothelial interactions were analyzed by videomicroscopy and analysis of covariance. Results Activation of neutrophils rendered adhesion increasingly dependent on shear stress reduction. At normal shear stress shedding of L-selectin decreased adhesion by 56 . Increased rolling fractions of activated PMN at low shear stress revealed impaired integrin affinity despite numerical up-regulation of CD11b. On sub-maximally activated intact HUVEC shear stress
