APPENDIX II 



A variation of this hypothesis, suggested by Professor 

 Okkels, involves also a vasoconstrictor substance (cf. 

 Hypothesis 3, page 171). 



American workers of the Bartelmez-Daron school, who 

 have not observed arteriovenous anastomoses in their ma- 

 terial, obtained chiefly from monkeys and prepared with 

 great care though by methods differing from those of the 

 Danish investigators, are naturally doubtful of hypotheses 

 that depend upon the arteriovenous shunts. 



Other possible mechanisms that have been hinted at, but 

 not as yet supported by thorough anatomical demonstration, 

 depend upon supposed peculiarities of the walls of the endo- 

 metrial arteries, which are indeed somewhat different in 

 microscopic structure from those of other organs. It is 

 thought, at least vaguely, that their general structure re- 

 quires in some way the support of estrogenic hormones, or 

 that there are special points or regions on the arteries which 

 are sensitive to hormone fluctuations and thus serve as 

 sphincters to shut off arterial flow. 



Enough has been said to show that while the relation 

 of the uterine arteries to the menstrual process is still un- 

 solved, the question is being actively studied and we may hope 

 for better knowledge by the next time this book requires re- 

 vision. 



Note 14 (page 172, line 17) . Toxin theory of menstruation. 

 O. W. Smith and George Van S, Smith have modified their 

 conjectures about the cause of the menstrual breakdown of 

 the endometrium. As explained in an article in Clinical 

 Endocrinology^ 1946, vol. 6, they suggest that catabolic 

 changes of the endometrium resulting from reduction of estro- 

 gen at the end of the cycle cause the formation of a toxic 

 substance which damages the finer blood vessels and thus 

 brings on the menstrual necrosis and hemorrhage. 



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