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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. [ABSTRACT FROM AUTHOR]

Minor tranquilizers have been shown to be specific inhibitors of the elevation of plasma corticosteroid levels in rats subjected to mild stress. The inability of several anxiolytic compounds to show activity at high doses prompted an investigation of the effect on corticosteroid levels of these drugs over a wider dosage range. It was found that at high doses, the drugs themselves cause an elevation of corticosteroid levels masking the blocking of the stress-induced elevations. It was discovered that upon sub-chronic administration, the drug-induced elevation diminishes while the ability to inhibit stress-induced elevation persists. Finally, an extensive dose response curve for phenobarbital demonstrated a variety of responses, depending upon the dose; an antistress effect at low dose, a relatively ineffective dose range from 50-100 mg/kg, and a corticosteroid lowering effect at anesthetic doses. The lack of effect of moderately high doses has been explained through their depressant side effects, which in themselves are stressful to the animal.