Thrombosis and its significance after experimental pulmonary thromboembolism

To study thrombosis and its significance after acute experimental pulmonary thromboembolism.

The acute pulmonary thromboembolism (PTE) model of rabbits was established by intravenous injection of autologous blood clots (0.04 g/kg) which were stabilized in temperature-controlled (70 degrees C) distilled water for 10 min. The process of thrombosis was observed grossly and microscopically. The Quick's method was used to examine the coagulability of blood and radioimmunoassay was employed to measure the level of plasma thromboxane A(2) and endothelin.

Thrombotic propensity was observed at 1 h, fresh thrombus started to form and the blood coagulation system was activated at 24 h following clots infusion. Emboli were completely or partly dissolved at 5 d and appeared to organize at both 10 d and 14 d after clots were infused. Venous plasma thromboxane A(2) concentration began to increase at 5 min (2489.59 +/- 714.68 ng/L) and reached its maximum at 15 min (2545.46 +/- 590.58 ng/L) then declined at 60 min after clot infusion (P < 0.001, respectively, vs 626.59 +/- 510.02 ng/L of pre-clot). The level of endothelin in both arterial and venous blood increased at 5 d post-clot infusion (840.74 +/- 154.19 ng/L, 230.35 +/- 52.39 ng/L, respectively) compared to the one before infusion (602.66 +/- 453.26 ng/L, 148.01 +/- 53.28 ng/L, respectively, P < 0.05).

Thrombosis occurs after autologous-blood-clot-induced PTE. The interactions between thrombus formation, fibrinolysis and organization determines the consequences of emboli. Abnormalities of endothelin metabolism and the increment of thromboxane A(2) may play an important role in PTE.