The uterine arteries are the primary vessels supplying oxygenated blood and nutrients to the uterus. These paired arteries, one on each side, have a dynamic role that changes dramatically depending on a woman’s physiological state. Their function is intimately tied to the cyclical preparation and maintenance of the uterine lining, and they undergo a remarkable transformation during pregnancy to support a developing fetus.
Anatomy and Baseline Function
The uterine artery originates as a branch of the internal iliac artery deep within the pelvis. It runs inferiorly and medially within the broad ligament, a double-layer of peritoneum that supports the uterus. A clinically important anatomical relationship is the artery crossing over the ureter, the tube carrying urine from the kidney to the bladder, often described by the phrase “water under the bridge.”
Upon reaching the side of the uterus near the cervix, the vessel divides into ascending and descending branches. The ascending branch travels upward along the lateral border of the uterus in a coiled manner, allowing the vessel to stretch as the uterus expands. This branch gives rise to arcuate arteries that encircle the uterus, which then penetrate the uterine muscle (myometrium) as radial arteries.
The radial arteries terminate as the straight and spiral arteries that supply the endometrium. In the non-pregnant state, the spiral arteries are highly responsive to hormonal fluctuations. A drop in progesterone triggers the constriction of these vessels, leading to temporary oxygen deprivation and the shedding of the functional layer of the endometrium (menstruation).
Transformation and Role in Pregnancy
During pregnancy, the uterine arteries must undergo an extraordinary transformation to meet the metabolic demands of the growing fetus and placenta. The spiral arteries, which are muscular and narrow in the non-pregnant state, change the most dramatically. This change is orchestrated by extravillous trophoblast cells, originating from the developing embryo, that invade the uterine wall.
These invasive trophoblast cells migrate into the walls of the maternal spiral arteries, replacing the muscular and elastic tissue with a non-contractile, fibrinoid material. This physiological remodeling converts the narrow, high-resistance arteries into wide, funnel-shaped conduits. The transformation ensures the vessels lose their ability to constrict and become unresponsive to maternal blood pressure regulation.
The result is a low-resistance, high-volume blood flow pathway that delivers a constant supply of maternal blood directly to the placenta, irrespective of short-term changes in the mother’s blood pressure. This constant flow ensures the efficient exchange of oxygen, nutrients, and waste products between the maternal and fetal circulations. The conversion process is normally complete by the end of the second trimester.
When trophoblast invasion and subsequent arterial remodeling is incomplete, the spiral arteries retain muscular, contractile properties. This failure results in persistently high resistance to blood flow, leading to inadequate placental perfusion and a reduced supply of oxygen and nutrients to the fetus. This impaired transformation is considered the underlying cause of severe pregnancy complications, including preeclampsia and Intrauterine Growth Restriction (IUGR).
Uterine Artery Embolization for Fibroids
Uterine Artery Embolization (UAE), sometimes referred to as Uterine Fibroid Embolization (UFE), is a minimally invasive procedure used primarily to treat symptomatic uterine fibroids. Fibroids, which are non-cancerous growths of muscle tissue, rely heavily on the uterine arteries for their blood supply. This vascular dependency is exploited to cause the fibroids to shrink.
The procedure is performed by an interventional radiologist who accesses the patient’s arterial system, typically through a small puncture in the femoral artery in the groin. Using specialized X-ray guidance (fluoroscopy), a catheter is threaded through the major arteries until it reaches the left and right uterine arteries.
Once the catheter is correctly positioned, the radiologist injects tiny embolic particles directly into the vessel. These microscopic spheres, often made of materials like polyvinyl alcohol or gelatin, are designed to permanently lodge in the small arteries that supply the fibroids. This intentionally blocks the blood flow.
The fibroid tissue, which lacks the robust collateral blood supply of the healthy uterine muscle, becomes starved of oxygen and nutrients. This deprivation causes the fibroid cells to die through a process called infarction, leading to a significant reduction in fibroid size and improvement in symptoms. The healthy uterine wall tissue recruits dormant collateral vessels to maintain its blood supply, preventing widespread damage.