[Myocardial oxygen consumption].
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Biomedical subjects
Publications and source records attributed to J Moravec.
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Light and electron microscopy, combined with morphometry, were utilized to study myocardial cell modifications induced by a temporary abdominal aortic constriction in the rat. During the early stage of active hypertrophy, cell enlargement in the subendocardial layers of the left ventricle was predominant. This enlargement may be partly due to intracellular edema, characteristic of cell damage. Degenerative foci leading to fibrous scars were found primarily in the subendocardium and midwall layers. The times taken by the different cell structures to adapt to modifications of the load were rather different; some adapted very rapidly (nucleoli, intercalated discs), while others were much slower (cell diameter, mitochondria).
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The left ventricle myocardium of rats subjected to a two steps mechanical overloading (abdominal aorta constriction + aortic insufficiency) was examined in the light and electron microscopes at several stages of the load, and particularly after 3 to 6 months when the animals exhibited congestive heart failure. In these conditions, the heart weight exceeded the control by more than 100%. In the later stages, the absence of parallelism between heart weight and cell diameter was compatible with a process of hyperplasia. Cellular lesions looking like recent were found more and more frequently with time. Within apparently normal cells proliferation of small mitochondria, nucleoli and Golgi apparatus are compatible with some deficit in energy balance, which is usually encountered only in early stages of the load.
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