ULTRASTRUCTURE OF MYOCARDIUM AFTER PULMONARY-EMBOLISM - STUDY IN RAT

  • 1 January 1978
    • journal article
    • research article
    • Vol. 92  (2) , 421-458
Abstract
Whether acute massive pulmonary embolism can produce myocardial changes visible by EM light microscopy was studied. Pulmonary embolism was produced 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 3-15 h (these rats were killed after 1 h), and sublethal embolism with a dose compatible with 100% survival (these rats were killed after 24 h). In both groups, the left ventricle was normal. The right ventricle showed 2 types of changes: a distinctive lesion of the myocytes, more diffuse after lethal embolism and different from the zonal lesion of shock. It consisted primarily in a localized shredding of the myofibrillar system; 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. Necrosis was already apparent at 1 h and was more extensive after 24 h. 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 capillaries 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 known as miliary infarcts and myocytolysis. A factor or common to all 3 may be the preservation of the microcirculatory vessels and the experimental model helps illuminate the pathogenesis of the human lesions. The right ventricle of acute cor pulmonale may develop cellular changes with a complex pathogenesis (mechanical, ischemic, and possibly hormonal). The nature of the changes found in the model could represent the morphologic substrate of right-sided failure; it can be correlated with the ECG abnormalities found in the comparable human condition.