Impact of leukocytapheresis on the coagulation and lung injury in the endotoxemia dogs

Abstract

To explore the role of leucocyte in the coagulation and fibrinolysis system in endotoxin-induced lung injury, the impact of peripheral leukocytapheresis (LCAP) on the coagulation and fibrinolysis system, and the lung injury in the endotoxemia dogs were observed. Endotoxemia was introduced in dogs with lipopolysaccharidea (LPS, 2 mg/kg). A total of 30 dogs were randomly assigned into LPS group (dogs were treated with LPS alone), sham group (dogs underwent LPS treatment and then sham LCAP 12-14 h later) and LCAP group (dogs underwent LPS treatment and LCAP 12-14 h later) (n=10 per group). The levels of peripheral activator protein C (APC), soluble thrombomodulin (sTM) and plasminogen activator inhibitor-1 (PAI-1) were measured 0 h before LPS treatment and 2, 6, 12, 14, 16, 24 and 36 h after LPS treatment. Result showed that the serum level of APC at 14 and 16 h after LPS treatment in LCAP group was significantly higher than that in LPS group at corresponding time points (P<0.05). The serum levels of sTM and PAI-1 at 14 and 16 h after LPS treatment in LCAP group was significantly lower than those in LPS group at corresponding time points (P<0.05). The incidence of lung injury in LCAP group was lower than that in LPS group (P<0.05). At the early stage of endotoxemia, LCAP can improve the balance of coagulation and fibrinolysis which may partly contribute to the improvement of oxygenation index and attenuation of lung injury. Key words: Endotoxemia, leukocytapheresis, coagulation/fibrinolysis.