1598 HANDBOOK OF PHYSIOLOGY ^ CIRCULATION II 



VEINS 



ARCUATE VEIN 



fig. 12. Pattern of veins draining basal plate of placenta in the monkey at various stages of 

 pregnancy. [Permission of Ramsey (181).] 



other vascular bed increases so that it receives a larger 

 portion of the incoming arterial blood to the uterus. 



MENSTRUATION 



The morphological and physiological mechanisms 

 of menstruation have been the subject of considerable 

 interest, particularly since precise knowledge of 

 uterine rhythmic cycles was first established some 

 forty years ago. Reviews on the subject in a modern 

 context began to appear when Hartman (96) dis- 

 cussed the subject of intermenstrual bleeding. 

 Bartelmez (23) gave us the first comprehensive re- 

 view of the subject, however, and this was extended 

 and revised in the light of later information by 

 Reynolds (196), by Smith & Smith (222) and by 

 Kaiser (124). Since that time, remarkably little 

 attention has been directed to the problem. 



In the uteri of certain but not all primates there are 

 numerous coiled arterioles in the endometrium [Daron 

 (62), Dalgaard (59), Kaiser (121), Bartelmez (26)] 

 which are demonstrable in conventional tissue sec- 

 tions [Kaiser (121)]. These arterioles undergo in- 

 crease in coiling throughout the menstrual cycle, 

 reaching maximum development prior to menstrua- 

 tion [Daron (62), Kaiser (121)]. Van Wagenen (237) 

 notes that it is vasoconstriction of these vessels [not 

 coiling, as commonly supposed (61)] which causes 

 ischemia. Then, due to hormonally induced changes 

 within the tissues [Smith & Smith, (222)], there is 

 loss of tissue fluid and thinning or regression of the 



endometrium, and this results in congestion and 

 stasis of blood in the coiled vessels [Markee (144)]. 

 Subsequently, the superficial layers of the en- 

 dometrium degenerate, slough off in an irregular but 

 spreading manner as menstruation takes place. 

 Sloughing begins when the endometrium is about 

 one-half of the peak thickness prior to the end of the 

 cycle. Bleeding is by capillary seepage, by reflux 

 venous hemorrhage [Markee (144), Daron (63), 

 Bartelmez (22)], and occasionally by brief arterial 

 spurting of blood [Markee (144)]- Menstruation 

 begins in localized areas and extends to others to 

 involve the entire area [Strassman (228), Phelps 

 ( 1 72)]. A role of arteriovenous shunts in the menstrual 

 process is both alleged [Schlegel (216), Dalgaard 

 (59)] and denied [Bartelmez (24)], but the evidence 

 at hand seems to favor the former view [see Hertig 

 & Rock (104)]. The physiological effect of coiling the 

 arterioles of the uterus can hardly be different from 

 that of coiling of vessels in the ovary and the testicle. 

 Here, it lowers the blood pressure to the tissues beyond 

 the coil [Reynolds (200), Waites & Moule (240)]. 



Since menstruation has been shown to be asso- 

 ciated with local hemodynamic changes within the 

 tissues concerned, some investigators have attempted 

 to induce profound hemodynamic disturbances with a 

 view to causing uterine bleeding. This has been done 

 [Van Wagenen & Zuckerman (238), Markee et a!. 

 (145)] but not invariably so [Emmel et al. (69)]. The 

 effect of cord transection depends upon a proper 

 effective estrogen level. 



The critical factors in determining what manipula- 



