Abstract
Attempts were made to clarify the mechanism with which the pulmonary infarction occurs, from coagulation-fibrinolytic point of view.
Pulmonary infarction was produced in 77.8% of the rabbits by infusion of human blood clots 2 days after intravenous injection of Lycopodium spores, in 28.6% or 55.6% of those by infusion of human blood clots on the 2nd or 3rd day after intravenous injection of minced human thrombi, and in 50.0% of those by infusion of rabbit blood clots on the 3rd day after intravenous injection of minced rabbit thrombi.
The group of rabbits with the pulmonary infarction showed more marked increase in the coagulative activity and reduction in the fibrinolytic activity on the 2nd or 3rd day after the 1st injection of Lycopodium spores or minced thrombi of either human or rabbits origin, than that in the animals without it, and in the former group a more pronounced consumption of the coagulation factors 3 hours after the 2nd injection of the clots, and increases of fibrinogen and FDP were recognized from the 1st day afterwards. A plateau type pattern of changes in the fibrinolytic activity was frequently observed during the course of the pulmonary infarction.
