elye, Hans; Bajusz, E�rs
December 1959
Angiology;Dec1959, Vol. 10 Issue 6, p412
Academic Journal
Experiments on rats were performed to examine the effect of sodium deficiency upon various experimental cardiac lesions, which differ widely from each other in both their causative agents and their histologic characteristics. It was found that sodium deficiency significantly protected the heart against the production of necrosis, inflammation and/or calcification by dihydrotachysterol (DHT), plasmocid and papain. In fluorocortisol conditioned, sodium deficient animals the cardiac necrosis eliciting effect of neuromuscular effort was also markedly inhibited. A reduction of the severity and incidence of the �spotty myolysis� normally due to the administration of noradrenaline and vasopressin was suggestive, but not statistically significant. On the other hand, combined administration of DHT + calcium acetate produced fatal, acute suppurative myocarditis of an equal degree in the (control and sodium deficient rats. Thus, the protective effect of sodium deficiency against the calcifying and necrotizing actions of DHT was completely abolished by the concurrent administration of calcium acetate. The importance of sodium in the pathogenosis of cardiac necroses and the possible role of electrolyte-steroid interactions in calcifying and necrotizing cardiac diseases are briefly discussed on the basis of those and previous observations.


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