Objectives: 

Platelet-activating factor (PAF) is a significant phospholipid mediator of the immune system produced by a veriety of cells involved in inflammatory reactions in sepsis. PAFRA was demonstrated to have potent anti-inflammatory activity and survival benefit. During endotoxaemia, lipopolysaccharide (LPS, endotoxin) and proinflammatory cytokines trigger the development of disseminated intravascular coagulation (DIC). DIC is a potentially devastating complication of several diseases such as intestinal disease, sepsis, metritis, mastitis, and pneumonia. In this experimental study, our aim was to investigate the role of PAFRA on haemostatic disturbances in LPS-treated rats.

Materials: 

A total of 32 adult male Wistar rats (weight range: 200– 250 g) were divided into four equal groups: Group 1 served as negative control (C). Animals in Group 2 were given lipopolysaccharide (Escherichia Coli LPS, 0.111:B4, Sigma L4130) intravenously (1.6 mg/kg). In Group 3, PAFRA (10mg/kg, Sigma G6910) was injected intraperitoneally. In Group 4, PAFRA (10mg/kg IP) and LPS (1.6 mg/kg IV) were administrated simultaneously. Blood samples were collected 6 h after treatment.

Results: 

In rats with endotoxin-induced DIC (Group 2), platelet count, fibrinogen and antithrombin III levels (ATIII) were decreased, and activated partial thromboplastin time (APTT) and phrotrombin time (PT) were prolonged, leukopenia and significant changes in the leukocyte differential were evident. In addition, LPS caused statistically significant increases in D-Dimer, thrombin-antithrombin complex (TAT), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) compared to control group (P<0.05). PAFRA was not effective against the adverse effect of LPS (P>0.05) in group 4, as judged from hemostatic disturbances in this endotoxaemia model.

Conclusions: 

at the administered dose and route, PAFRA cannot be seen to have any useful effect on the pathogenesis of DIC in endotoxemia.