Electrocardiograms of rats maintained on selenium-low diets show the early development of a characteristic abnorinality. The change in the ECG pattern becomes very marked as death approaches, although animals probably do not die directly of heart failure. Histological changes seen in the cardiac muscle of these animals suggests that the abnormal ECG pattern is related to a change in the properties of the muscle fibres rather than the electrolyte disturbances, or other changes in plasma constituents.Plasma electrolyte determinations in these rats developing abnormal ECG's included Na, K, Ca, and Mg; all values were within normal limits as compared with animals receiving the same diet though supplemented with selenium, in which abnormal ECG's did not occur. Evidence is also presented that blood glucose levels cannot explain the ECG abnormalities. a THE prime purpose of this paper is to report certain characteristic changes found in the ECG pattern of rats maintained on diets low in selenium. Such diets are known to cause muscular dystrophy in a variety of animals, and both cardiac and skeletal muscle are affected in a manner which varies greatly from one species to another [Schwarz, 1961]. The dominating feature of selenium deficiency in the rat has been dietary necrotic liver degeneration [Schwarz, 1958]. However, the same diet fed to lambs caused marked dystrophic, and even necrotic changes in both the skeletal and cardiac muscle, whilst the liver remains reasonably normal, as judged by macroscopic and microscopic examination [Godwin, publication in preparation].The common denominator in selenium deficiency appears therefore to be alterations in the musculature. Schwarz [1958] found respiratory decline in liver slices from animals fed selenium low diets. These changes were detected between the 11th and 21st day of the experiment, the actual hepatic necrosis being a terminal phase. It seems to be important therefore to know more about the early changes occurring in the selenium-deficient animal, particularly with regard to changes in muscle, in order to gain insight into the fundamental role of selenium.The ECG abnormalities reported here occur early in the deficiency syndrome and are probably related more to changes in the properties of the cardiac muscle itself, rather than to electrolyte or other changes in plasma constituents. 282

Experimental selenium deficiency has been studied in a group of lambs weaned early on to a semi-synthetic diet. Nineteen lambs were used; eleven became selenium deficient, the remaining eight were supplemented with selenium and remained normal. Well-defined differences, in terms of histopathological changes, developed between the two groups. The dystrophic lesions were mainly found in skeletal and cardiac muscle, and to a lesser extent in the pancreas and diaphragm.Electrocardiograms showed the progressive development of a characteristic abnormality, after the animals had been on the deficient diet for a few weeks. Just before death the ECG pattern became grossly abnormal in some cases, a rise in the T-wave giving way to an elevated S-T segment, similar to that seen frequently in myocardial infaretion in man.Paralleling these changes, at least in time, there was a fall in blood pressure especially marked in the limbs, but present to a lesser degree in the rest of the systemic circulation. Taken together, these observations point to the possibilitv that the fundamental change occurring in selenium deficiency may be circulatory failure.Finally, comparison of the histopathological picture of the lamb and the rat, when both species are reared on the same diet, indicates that entirely different syndromes appear, at first sight, to develop. However, ECG changes previously studied in rats are somewhat similar to those reported here. Skeletal muscle is severely dystrophic in both species. Perhaps subsequent studies will demonstrate that even though the final outcome of selenium deficiency in different species is variable, the initial lesions are closely comparable.AT a recent symposium on the metabolism of vitamin E and related substances [Karrer et al., 19621, it was re-emphasized that though the metabolic functions of selenium and vitamin E are apparently closely related, neither can invariably take the place of the other. As their functions are as yet not clearly understood, the metabolic origins of certain well defined metabolic lesions are at present unsatisfactory. Muscular dystrophy induced by feeding large quantities of unsaturated fatty acids to lambs, for instance, responds well to vitamin E supplementation, though not to selenium [Welch et al., 1960]. On the other hand muscular dystrophy produced in poultry by feeding a diet low in selenium and vitamin E is prevented completely by selenium supplementation but is unaffected by additional vitamin E [Scott, 1962].'The following experiments were designed to produce in lambs and rats an uncomplicated selenium-deficiency syndrome, so that means could be sought to recognize the symptoms of the condition in its early stages.One of the striking features of vitamin E deficiency is the great variation of the pathological state which results in different species. Schwarz [1961] 94

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