UTERINE BLOOD FLOW 



l60I 



EMBARAZO NORMAL DE TERMINO 

 PARTO INDUCIDO PITOCIN l/V p^ U. por min 



EMBARAZO NORMAL DE TERMINO 

 PARTO INDUCIDO PITOCIN l/V ,-?r n U. por min 



DECUBITO DORSAL 

 mmHg f£\ 



N.510 



^VA jf^VENA 



DECUBITO 

 mmHg 

 30 



200 

 LATERAL DERECHO 



ILIACA 



PRESION 

 AMNIOTICA 



VENA CAVA 



W SUPERIOR 



PRESION 

 ARTERIAL 



minulos 



N.510 



VENA 

 ILIACA 



PRESION 

 AMNIOTICA 



VENA CAVA 

 SUPERIOR 



PRESION 

 ARTERIAL 



! minutos 



fig. 14. Effect of body position on pressure in the iliac vein, superior vena cava during late 

 pregnancy and arterial blood pressure. .4.- on back. Note bimodal pressure peaks. B: on side. Note 

 single simultaneous pressure peaks in upper and lower vena cava, synchronous with acme of uterine 

 contractions and lower systolic blood pressure. [Permission of Caldeyro Barcia el al. (51).] 



uterus becomes less hyperemic and gradually loses its 

 contractility [Reynolds (191)]. Within an hour after 

 estrogen is injected there is an intense hyperemia 

 [Markee (142), Pompen ( 1 76)]. Twelve or more hours 

 later the myometrium becomes active [Reynolds 

 (190)]. Beginning activity depends upon synthesis of 

 actomyosin in the uterus [Csapo (57)]; this is related 

 to a rise of aerobic metabolism of the uterus [MacLeod 

 & Reynolds (140)]. There seems to be an assumption 

 that this is solely in the smooth muscle of the myo- 

 metrium. It is possible, however, that smooth muscle 

 in the uterine blood vessels is equally estrogen- 

 dependent; this has not been investigated. Certainly, 

 with prolonged estrogen withdrawal the blood vessels 

 of certain parts of the uterine vasculature show a 

 reversible hyaline degeneration [Okkels & Engle 

 (163), Kahn & Laipply (.119)]. All parts of the vas- 

 culature are not equally affected. The very first 

 effect of estrogen on the uterine vasculature is to 

 cause capillary dilation [Pompen (176), Fagin & 

 Reynolds (74)]. Its role in affecting the larger vessels 

 seems to have attracted very little attention although 

 stilbestrol raises the arterial pressure in female but not 

 in male rats [Hill (106)]. 



When estrogen given to rabbits is combined with 



progesterone in relatively massive doses, profound 

 hyperemia of the uterus cccurs [Gillman (84)]. 

 Extensive sloughing of the endometrium results. 

 Estrogen alone increases capillary permeability 

 [Hechter et al. (99)] which is associated during the 

 first 6 hours with an increase in the relative wet 

 weight of the uterus of ovariectomized rats. Later the 

 relative dry weight increases progressively to a maxi- 

 mum about 24 hours after the injection [Astwood 



(13)]- 



The mechanism of the estrogen-induced hyperemia 



is indicated by the fact that estrogen increases the 

 acetylcholine-content of rabbit uteri within 1 hour 

 [Reynolds (193)], and its concentration in the uterus 

 changes during pregnancy [Reynolds & Foster (205)]. 

 One group of workers failed to confirm the response 

 in rabbits [Emmens et al. (70)] for unknown reasons. 

 Even so, estrogen seems to affect the acetylcholine of 

 the uterus by altering its cholinesterase content 

 [Herschberg (103), Sawyer & Everett (215), Everett 

 & Sawyer (73)]. Pompen (176), it will be recalled, 

 found that the uterus in situ does not become hypere- 

 mic under estrogen if atropine is administered. Kaiser 

 (125), however, failed to observe this if the endo- 

 metrium is transplanted, and without an innervation. 



