The basis was established for a rational sex hormone therapy with the isolation of the estrogenicl 2 sand androgenic hormones.3 It has been demonstrated by animal experiments that a basic effect of the sex hormones is hyperemization of the whole organism.4 4 When this observation was confirmed with regards to the skin in the 1930's in patients treated for well defined gonad insufficiency, the possibility then existed of treating patients with diseases of the circulatory system with sex hormones.In studies using animal experiments it has been possible to demonstrate a hyperemitising effect of both estrogenic and androgenic hormone. 5 These experiments suggest that the effect of the hormones is local and due to the liberation from the tissue of acetylcholine, which again has a dilating effect upon the blood vessels.Large doses of ergotamine tartrate cause necrosis of the tail in white rats, and this can be counteracted to a large degree by the simultaneous administration of sex hormone. 6 It has been possible to demonstrate plethysmographically that the administration of androgens to castrated men quickly results in an increase in the finger volume and that this is in some cases accompanied by a substantial increase in the temperature of the finger. None of these changes in the circulation of the finger is castrated men could be brought about by estrogenic hormones; however, these result in a considerable increase in finger volume in normal men. In women around the menopause a similar increase in the finger volume can be seen after the administration of estrogens.Even though a direct connection between a disturbance in the hormone production (gonad and adrenal cortex) and arteriosclerosis is unlikely, both clinical and biochemical factors suggest that both androgens and estrogens are of importance in the pathogenesis of arteriosclerosis. The indirect effect of the sex hormones on the various lipoid protein fractions of the blood, in which bound cholesterol is to be found, is presumably most important in this connection. An increase in the concentration of heta-or low density lipoproteins appears to occur in all the conditions that promote the development of arteriosclerosis. More beta-lipoprotein and less alpha or high density lipoprotein is found in the plasma of men than in the plasma of adult women of the same age. Androgens reduce the amount of alphaprotein whilst estrogens increase it. However, the concentration of beta-
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