i Goo 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION 



fig. 1 3. Schematic representation of arterial 

 supply to portions of uterus simplex (monkey, 

 human). [From Reynolds (.196).] 



Spiral Artery 

 Venous Lake 



Gland 



Capillary bed 

 Basal Artery 



Radial Artery 

 Arcuate Artery. 



Arcuate Vein 

 Peripheral Artery 



Functtonal 

 ENDOMETRIUM 



Basal 



Myo-Endometnal 

 border 



MYOMETRIUM 



& Schild (212)], while an induced higher blood 

 pressure has an opposite effect. Ahlquist & Wood- 

 bury (2) found in cats that when intrauterine pressure 

 reaches 60 to 70 mm Hg, uterine blood flow virtually 

 ceases. This is reminiscent of the report by Moir 

 (156) that when intrauterine pressure exceeds arterial 

 blood pressure, a woman feels ischemic uterine pain. 

 It may be that myometrial smooth muscle acts in 

 concert with that of the uterine blood vessels them- 

 selves. In myometrial studies, adrenaline and nor- 

 adrenaline cause decreased uterine blood flow in 

 rabbits and guinea pigs, associated with uterine con- 

 tractions [Dornhorst & Young (67)], but an action on 

 uterine blood vessels was not eliminated. The conse- 

 quence of strong uterine contractions on the systemic 

 circulation are shown by the fact that undulatory 

 changes in arterial blood pressure occur as the post- 

 partum uterus contracts [Franklin (82)]. 



For many years, speculation existed concerning 

 the effect of uterine contractions on the flow of blood 

 in the placenta of the human. Two possibilities 

 existed: a) that the contraction squeezes blood out of 

 the placenta as water may be squeezed out of a 

 sponge [Kermauner (128), Grosser (89, 90)], and 

 b) that as the intervillous space pressure builds up, 

 veins are at first occluded, then pressure increases in 

 the intervillous space as it increases in the amniotic 

 cavity [Keiffer (127), Wagner (239), Pryztowski 

 (179)]. Meanwhile, blood remains in the placenta to 

 meet the needs of maternal-fetal exchange during 

 uterine contraction. There is now no doubt that the 

 second view is correct. This was suggested indirectly 

 by the work of Woodbury et al. (250) and shown 

 clearly by Woodbury et al. (251 ), Alvarez & Caldeyro 



Barcia (3), Caldeyro Barcia (50), and by Pryztowsky 

 (179) in women and by Ramsey et al. (188) 

 n monkeys. 



BODY POSTURE AND UTERINE CONTRACTILITY 



Perhaps the most telling observation about the 

 effect of uterine circulation on uterine contractions is 

 the observation made in women that a change in 

 posture modifies the quality of uterine contractility. 

 When a woman in late pregnancy or in labor lies on 

 her back, uterine contractions of a given frequency 

 and intensity (i.e., change of intrauterine pressure) 

 are seen [Williams (246), Caldeyro Barcia et al. (51)]. 

 When she assumes a semireclining posture, or turns 

 on her side, the contractions become slower and more 

 intense. With a view to studying the role of compres- 

 sion of the inferior vena cava in the recumbent 

 position, pressures were recorded simultaneously in a 

 woman in the lower and upper parts of the vena 

 cava [Caldeyro Barcia et al. (51)]. The weight of the 

 gravid uterus on the retroperitoneal surface caused a 

 disassociation of the venous pulse pressures in the two 

 parts of the vein; with the woman on her side, the 

 venous pulse waves became synchronous, and the 

 quality of uterine contractions changed. 



ESTROGEN AND UTERINE BLOOD VESSELS 



Another indication of the relation between uterine 

 contractility and uterine blood flow lies in the ob- 

 servation that, following estrogen withdrawal, the 



