George B. Wislocki 639 



lactors as being responsible for the atrophy of the blood siipjjly to the antlers; 

 these explanations assume in one way or another that the internal or external 

 xessels are gradually mechanically choked by bone which is deposited around 

 them. Macewen adopts the belief, current amongst naturalists and hunters, 

 that the external blood supply of the velvet is obliterated by compression of 

 the large vessels of the velvet at the base of the antler by the gradual enlarge- 

 ment of the bony corona. Caton presents various reasons why these vessels are 

 not compressed in that way, and offers, instead, the explanation that the in- 

 ternal and external sets of vessels are directly obliterated by gradual closure 

 of the smaller radicals in the Ha\ersian canals and marrow spaces, due to the 

 pressure of accumulating deposits of lime salts. 



These theories in\olving local factors are based, however, more upon as- 

 sumptions than upon any adequate histological proof. Vascular injections 

 made by Rhtnnbler,"" as well as several which I have prepared," indicate that 

 the blood supply reaches the antler almost exclusively by the external vessels 

 in the velvet, whereas the internal stipply reaching the antler through its base 

 is almost negligible. Thus the characteristic, dense calcification of the interior 

 of the antler base is probably not responsible for the occlusion of any impor- 

 tant larger blood vessels. Although Caton's and Macewen's concepts are poorly 

 substantiated, it does not necessarily follow, as postulated by Olt, that atrophy 

 of the velvet must be hormonally controlled; it is still conceivable that, in 

 some as yet undisclosed way, local factors may be directly responsible for in- 

 terruption of the circtdation. Nevertheless, the idea of hormonal control is 

 inviting. In favor of it one might cite the slender parallels that the testes are 

 known to exert effects upon certain vascular beds, for example, upon the 

 vessels of the cock's comb (Hardesty""), as well as upon the human skin (Edwards 

 and co-workers'"*). 



The eventual loosening and shedding of the dead antler, on the contrary, 

 appear more definitely to be hormonally determined. At this period the pedicle 

 becomes exceedingly hyperemic and the bone undergoes marked resorption, 

 especially at the line of jtmction of the antler with the apex of the pedicle 

 (von Korff,-" Macewen,"' Wislocki''). This event occius normally during the 

 period of gonadal involution. Moreover, in deer castrated after the antlers 

 are dead, the horns are shed prematurely within one to fotn- weeks following- 

 removal of the gonads. Hence, the casting off of the antlers appears to be due 

 to withdrawal of testictdar hormone, resulting in a local hyperemia and 

 decalcification of the apices of the pedicles of the frontal bones. 



It has been pointed out that in all castrate deer, excepting the reindeer, the 

 antlers assume variable forms, reaching their most extreme expression in roe 

 deer in which bizarre masses of poorly calcified antler tissue arise. If castration 

 occurs soon after antler growth has commenced, the horns develop normally 

 up to the time when the influence of the testes ordinarily begins to express 

 itself. Only from then on do the horns begin to show the effects of gonadal 



