Abstract
Attempts were made to clarify the mechanism with which the pulmonary infarction occurs, from coagulofibrinolytic point of view.
The following results were obtained:
(1) Pulmonary infarction could be produced at such a high rate as 74.4% through infusion of blood clots 2 days after intravenous injection of Lycopodium spores, when the coagulation activity was on the highest grade and the fibrinolytic activity was on the lowest grade.
(2) Severe hemorrhage was observed in the post-mortem examination of the lungs 24 to 48 hours after infusion of the blood clots. The embolus remained thereafter, but the hemorrhage tended to diminish.
(3) Consumption of coagulative factors and fibrinolytic factors was observed in the pulmonary venous blood than in the pulmonary arterial blood 3 hours after infusion of blood clots. Consumption of the coagula-tive and fibrinolytic factors and increase of F.D.P. were observed 12 to 24 hours after the infusion, although there were more or less differences depending upon experimental methods.
(4) Consumption of free-type activator, increase of bond-type activator, and formation of marked focal lysis ring examined by means of fibrinolysis autograph were observed in tissue samples examined 24 to 48 hours after the infusion of blood clots.
(5) It was assumed that a close relationship exists between the production of pulmonary infarction and the disorders of the coagulation-fibrinolytic system, especially the fibrinolytic factors including those in the blood and tissue samples, mainly examined around 24 hours after infusion of blood clots.
