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American Journal of Pathology, Vol 92, 421-458, Copyright © 1978 by American Society for Investigative Pathology

REGULAR ARTICLES

Ultrastructure of the myocardium after pulmonary embolism. A study in the rat

HF Cuenoud, I Joris and G Majno

The purpose of this study was to find out whether acute massive pulmonary embolism can produce myocardial changes visible by light and electron microscopy. Ww therefore produced pulmonary embolism in rats using plastic microspheres (diameter, 15 +/- 5 mu). Two experimental protocols were used: lethal embolism, with a dose of microspheres known to kill in 3 to 15 hours (these rats were killed after 1 hour), and sublethal embolism, with a dose compatible with 100% survival (these rats were killed after 24 hours). In both groups, the left ventricle was normal. The right ventricle showed two tyes of changes: a) A distinctive lesion of the myocytes, more diffuse after lethal enbolism and different from the "zonal lesion" of shock. It consisted primarily in a localized shredding of the myofibrillar system; hence, the name shredding is proposed. Earlier stages of this lesion were represented by focal dissolution of the Z line (Z lysis). The pathogenesis of these lesions appeared to be primarily mechanical. b) Necrosis was already apparent at 1 hour and was more extensive after 24 hours. The pathogensis of the necrotic lesions is best explained by a temporary ischemia followed by delayed reflow; a possible potentiating role of endogenous catecholamines cannot be excluded. Most capilaries in the necrotic foci remained functional; this explains the rapid rate of the healing process of such lesions. A comparison is drawn between the observed foci of necrosis and the human myocardial lesions knowns as "miliary infarcts" and "myocytolysis." It is proposed that a factor common to all three is the preservation of the microcirculatory vessels and that our experimental model helps illuminate the pathogenesis of the human lesions. It is concluded that the right ventricle of acute cor pulmonale may develop cellular changes with a complex pathologenesis (mechanical, ischemic, and possibly hormonal). The nature of the changes found in our model could represent the morphologic substrate of right-sided failure; it can be correlated with the electrocardiographic abnormalities found in the comparable human condition.

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