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[Morphological changes in the lungs in myocardial infarct]
Arkhiv Patologii
|January 1, 1977
Summary
Myocardial infarction causes four lung lesion stages, from hypoatelectasis to bronchopneumonia. Enzyme activity in lung cells changes dynamically, decreasing early and recovering later, but drops again with bronchopneumonia.
Area of Science:
- Pathology
- Cardiology
- Pulmonary Medicine
Context:
- Investigates morphological lung lesions in rabbits with experimental myocardial infarction.
- Examines 17 fatal human cases with myocardial infarction at various post-onset intervals.
- Establishes a correlation between myocardial infarction progression and lung pathology.
Purpose:
- To characterize the sequential morphological changes in the lungs following myocardial infarction.
- To analyze the dynamic alterations in oxidative-reductive enzyme activity within alveolar cells during myocardial infarction.
- To identify how secondary complications like bronchopneumonia influence these enzymatic changes.
Summary:
- Identified four interrelated stages of lung lesions: hypoatelectasis, classical atelectasis, alveolitis, and bronchopneumonia.
- Observed a dynamic pattern in oxidative-reductive enzyme activity (succinate, malate, lactate dehydrogenase) in alveolar cells.
- Enzyme activity initially decreased, then recovered by the first week post-infarction.
- Complicated cases with bronchopneumonia showed a renewed decrease in succinate dehydrogenase activity.
Impact:
- Provides a detailed understanding of lung pathology secondary to myocardial infarction.
- Highlights the role of enzymatic changes in the lung's response to cardiac events.
- Offers insights into potential diagnostic or prognostic markers related to lung complications in myocardial infarction patients.