Abstract
Two main theories have been proposed related to the causation of the pulmonary thrombosis and infarction. The former one is proposed by Virchow and it justifies the mechanical obstruction of the distributing arteries and the latter one is recently offering a view that the functional derangement of the distributing arteries as the another noteworthy causative factor. The present study has been performed to evaluate the latter theory. The author has investigated 12 cases of the pulmonary thrombosis occuring in the main trunk of pulmonary arteries and 22 cases of pulmonary infarction and the following results were obtained.
1) The most conspicuous atheromatous changes were observed in the main trunk of the hilar region which were associated with organizing or organized thrombus.
2) It was postulated that the initiation of the early circulatory disturbance, being manifested by mechanical destruction of the vascular wall as well as imbibition of the serous component might play an important roll in causation of the changes. The causative mechanism of these circulatory disturbance will be essentially identical with these of heart, brain and kidneys which were previously reported by associates in this laboratory. In spite of the fact that these cases were involved in rather striking pathological changes they failed to show rather outspoken clinical manifestation. The discrepancy between them constitutes the most outstanding feature of these conditions.
3) The ectatic changes of the peripheral region as well as the vascular stasis and hemolysis also constitute the cardinal pathological changes, while the proximal portion reveal rather striking stenotic change which was induced by thrombotic adhesion to the intimal surface.
4) The most frequently encountered site for the pulmonary infarction is assumed to be the dorsal aspect of the lower lobe and localized in peripheral region. In spite of the occlusive mechanism in the proximal region, the distal portion is induced in ectatic process and prominent stasis.
5) Based on these observations, the pulmonary thrombosis occuring in the main trunk of the pulmonary arteries or pulmonary infarction may be resulted from the antecedent atherosclerotic changes which may be formed by persisting increased vascular resistence and increased intravascular pressure.
6) It is concluded that the far advanced circulatory derangement will be the most cardinal causative factor of the thrombosis and infarction and pathological significance of these findings are fully discussed in this communication.
