Direction of blood flow and changes in resistance of major arteries supplying the ovary of the pregnant rat

• Published in: Biology of reproduction Vol. 57; no. 1; pp. 43 - 48
• Main Authors: MASSA, H. M, BRUCE, N. W
• Format: Journal Article
• Language: English
• Published: Madison, WI Society for the Study of Reproduction 01-07-1997
• Subjects: Animals; Arteries - physiology; Biological and medical sciences; Blood Flow Velocity; Catheterization - instrumentation; Female; Fundamental and applied biological sciences. Psychology; Mother. Fetoplacental unit. Mammary gland. Milk; Ovary - blood supply; Pregnancy; Pregnancy, Animal - physiology; Pregnancy. Parturition. Lactation; Rats; Rats, Wistar; Uterus - blood supply; Vascular Resistance - physiology; Vertebrates: reproduction; Rat; Rodentia; Anastomosis; Uterine artery; Blood flow; Pregnancy; Vertebrata; Mammalia; Vascular resistance; Blood vessel; Female genital system; Female; Circulatory system; Hemodynamics; Ovarian artery
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod57.1.43

In this study, we examined changes in vascular resistance contributing to increased ovarian blood flow in the pregnant rat.
Ovarian blood flow was monitored in vivo using a venous outflow cannulation technique in nonpregnant rats and in pregnant
rats at Day 16 and Day 22, and increased from 0.18 +/- 0.02 to 0.81 +/- 0.09 and 1.02 +/- 0.08 ml min(-1) ovary(-1) (mean
+/- SEM; n = 7, 7, 6), respectively. Intrinsic vessels within the ovarian complex accounted for 81%, 73%, and 70% of total
resistance to ovarian blood flow. Of the two major extrinsic supply vessels, from one-half to two-thirds of the ovarian blood
was derived from the uterine artery, and the ovarian artery never contributed to uterine blood flow. These results indicate
that the major supply vessels are unlikely to limit ovarian blood flow, even near term when competing demand by the gravid
uterus reaches a peak. The finding that ovarian blood flow is derived predominantly from the uterine artery may relate to
local mechanisms that influence ovarian function and fetal growth.