thromboxane-b2 and Factor-X-Deficiency

Human isolated monocytes possess low levels of procoagulant activity, which was stimulated 10-30 fold by brief (2 hr) exposure to 10 micrograms/ml endotoxin. This activity was expressed in normal or factor XII-deficient plasma, but lost in plasma deficient in factors X or VII, indicating that it was due to thromboplastin. The stimulation of monocyte thromboplastin by endotoxin was inhibited in a dose-dependent manner by two phospholipase A2 inhibitors, 4-bromophenacyl bromide and quinacrine, and by two lipoxygenase inhibitors, eicosatetraynoic acid and nordihydroguaiaretic acid. Two cyclooxygenase inhibitors, aspirin and indomethacin, prevented endotoxin-induced increases in thromboxane B2 production but had no effect on thromboplastin production. These results suggest that a component in the sequence of lipid deacylation, arachidonic acid release, and metabolism via lipoxygenase may mediate the stimulation of monocyte thromboplastin activity by endotoxin.

Topics: Arachidonate Lipoxygenases; Arachidonic Acid; Arachidonic Acids; Cyclooxygenase Inhibitors; Endotoxins; Factor VII Deficiency; Factor X Deficiency; Humans; Lipoxygenase Inhibitors; Monocytes; Phospholipases A; Phospholipases A2; Thromboplastin; Thromboxane B2