Plasma fibronectin and resistance to thrombosis during sepsis

Previous studies have suggested that plasma fibronectin is a component of the physiological antithrombotic mechanism and is related to resistance to cardiopulmonary failure during sepsis. The current study addresses the hypothesis that fibronectin deficiency results in increased sensitivity to thrombosis during sepsis, whereas increased fibronectin results in enhanced resistance. Rats were injected with purified fibronectin, antiserum to fibronectin, antiserum to albumin or vehicle prior to intraaortic infusion of saline, live Escherichia coli (10(7)--10(8)/100 gm) or E coli endotoxin (0.001--0.1 mg/100 gm). Infusion of the higher doses was associated with greater mortality in antifibronectin groups than the other groups. Mean arterial blood pressure fell transiently in all groups following injection of antifibronectin but not following the other pretreatment. Both endotoxin and bacterial infusion resulted in severe thrombocytopenia in antifibronectin-treated animals and to a lesser extent following antialbumin. Fibrinogen consumption was increased in all groups after antifibronectin treatment in bacteria infused animals after pretreatment with antialbumin or fibronectin. Fibrin degradation products were increased by bacterial infusion in animals treated with either antiserum. The current data support a relationship between plasma fibronectin and resistance to thrombosis. The relationship was not as clear-cut as that previously observed for nonseptic thrombotic states.