Myocardial pathology in rats exposed to prolonged environmental heat

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Abstract
The aim was to assess the role of continuously high environmental temperature in the genesis of tropical cardiomyopathies. Rats were kept in a climatic chamber at a constant temperature of 34 degrees C (40% relative humidity) for 1 or 2 months. Controls were kept at 24 degrees C. The hearts, either taken directly from the animals or following Langendorff perfusion, were then examined by light and electron microscopy. 69 rats of two different strains, aged about 1 month, were used as the study group. There were 32 suitable controls. The weights of the heated rats and their hearts were lower than controls but the body to heart weight ratio was unchanged. The maximum pressure developed by the left ventricle was higher. With light microscopy, focal necrosis, lymphoid and mast cell infiltrations, fibrosis, and occasional calcifications were seen in most heat exposed rats. With electron microscopy most myocytes appeared normal when taken from whole animals. The additional trauma of heart suspension or hypo-osmolar perfusion caused severe membrane related pathology, while controls remained unaffected. Prolonged exposure to heat produces focal cellular reactions and disturbance of the myocyte membrane. The pathogenesis of the changes is as yet uncertain. It may be multifactorial and include calcium and/or oxygen derangements mediated by mast cells, catecholamines, hypothyroidism, and heat shock proteins.

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