Thrombo-embolic primary pulmonary arteriosclerosis.

That diverse factors are concerned in causing arterial pathological changes largely confined to lungs is clear from a review published by McKeown (1952). Only one of these factors, incorporation of fibrin into arterial intima, is here considered as a cause of pulmonary arteriosclerosis and cor pulmonale. Goedel (1930), Belt (1939), and according to Duguid (1946) Rokitansky were all aware that incorporation of blood clot into vascular intima produced lesions simulating arteriosclerosis. Duguid once more directed attention to this fact and following his lead, various workers undertook experiments to test his conclusions which were based on human autopsy material By injecting fibrin emboli intravenously into rabbits it has been shown that lesions like arteriosclerosis may be induced in small branches of the pulmonary artery (Harrison, 1948 and 1951; Muirhead and Montgomery, 1951; and Barnard, 1953). These workers used emboli prepared in vitro either from the animal's own blood or from blood of a different animal. Assuming that experimental thrombo-embolic arteriosclerosis has significance for man, primary pulmonary arteriosclerosis might be a disorder of the blood characterized by repeated and protracted pulmonary embolism by showers of minute clots originating in systemic veins, where conditions are favourable for intravascular coagulation. If such emboli formed in systemic venous blood, few would escape the pulmonary arteriolar and capillary filter and thus significant arteriosclerosis would be confined to the lungs. Embolic experiments that aimed at discovering the role blood clot plays in causing pulmonary arteriosclerosis would, however, have added significance if lesions were also brought about by injecting substances that would precipitate fibrin in circulating blood. Heard (1952) injected magnesium adenosine triphosphate together with Russell viper venom and studied arterial lesions so caused. McLetchie (1952) conducted similar experiments using Russell viper venom and thromboplastin extract. Others have recorded fibrin embolism ofpulmonary vessels using thromboplastin extract or highly diluted thrombin solution, but their object was the study of blood coagulation and not the arterial changes (Julrgens and Studer, 1948; Ratnoff and Conley, 1951; Page et al., 1951; and Schneider, 1951). Schneider has shown, moreover, that placental trauma to rabbits caused fibrin embolism severe enough to kill, and that in human abruptio placent, placental thromboplastin may enter the maternal circulation so causing fibrin embolism of the lungs, in some cases leading to death. This paper describes pathological changes in mouse and rabbit lungs due to thromboplastin extract injected intravenously: extract was not mixed with an unphysiological coagulant as in previous experiments of this kind. It also argues that protracted embolism by minute clots is one cause of primary pulmonary arteriosclersois and cor pulmonale in man.