抄録
Coagulation and fibrinolysis display important roles in various physiologic and pathologic conditions linked closely with kallikrein-kinin and complement systems and also with prostaglandin metabolism.
In this report, much emphasis is given to the pathophysiological significance and contributions of this system to the pathogenesis of pulmonary thromboembolism, disseminated intravascular coagulation syndrome, generalized Shwartzman reaction, experimental pneumonitis induced by anti-lung antibody, monocrotalin induced pulmonary hypertension, lung edema due to endotoxin and metastasis of lung cancer.
Recently, the frequent occurence of pulmonary thromboembolism has been widely recognized and we observed thrombi or thromboemboli in pulmonary arteries in 41.6% among autopsy cases aged 40 years or older. Although the effects of thrombolytic therapy are still controversial, a clear understanding of the thrombolytic process enables the clinicians to use thrombolytic agents more effectively. Using human artificial thrombi by the Chandler loop, we disclosed that urokinase itself activates directly plasminogen to plasmin on the fibrin threads in thrombi, a consequence of which causes thrombolytis. Based on these results, a larger dose of urokinase is recommended for thrombolytic therapy. The important role of plasminogen tissue activator of vascular endothelium is also emphasized.
The etiology of DIC was investigated in terms of the generalized Shwartzman reaction ultrastructually and it was revealed that infiltration and destruction of granulocytes in pulmonary vessels followed by release of procoagulant were the initial events in pulmonary vascular damage.
In experimental pneumonitis induced by anti-rat lung antibody, intravascular coagulation secondary to antigen antibody reaction in pulmonary capillary basement membrane contributes to the initiation of this disease.
Intravascular coagulation also contributes to the development of monocrotalin-induced pulmonary hypertension and pulmonary edema due to endotoxin. Emphasis is given here especially to the action of degradation products of fibrinogen and fibrin. Both fragments D and E are shown to have permeability-increasing activity in the pulmonary vascular bed. Even lower molecular weight degradation products of fibrin have a strong enhancing effect on vascular permeability.
Thromboplastic and fibrinolysic activities of tumor cells themselves are considered to be important factors in hematogenous metastasis. From the experimental observations it was concluded that the inhibition of coagulation and platelet aggregation and enhancement of fibrinolysis are recommended as a useful treatment for prevention of metastasis.
It is hoped that much information will be found in this report to achieve a better appreciation of the recent progress in the field of coagulation and fibrinolysis and of the etiology of various lung diseases so that a better clinical application of anticoagulant and thrombolytic therapy could be accomplished.