Uteroplacental vascularization

The intervillous space is considered as receiving the most important part of the uterine flow input (> 90%), reaching the placenta through the modified spiral arteries network. The low vascular resistance detected on the uterine arteries is thought to be due to the presence of the placental shunt. Using a 3D Colour Doppler technology (ATL 5000), a complex anastomotic and intra-myometrial network has been detected. This vascular network is always detected during the first 48 hours of after delivery. During this time, the placenta has been removed, the uterine muscle is contracted, a low resistance of the uterine flow is systematically detected. A extraplacental vascular component must be considered as taking a functional part in the foeto-maternal exchanges.     

Intervillous space during uterine contractions in human subjects: an ultrasonic study.

Six patients at term were examined by ultrasound during uterine contractions. The length, thickness, and surface of the placental area were found to increase during uterine contraction compared to relaxation. The conclusion is drawn that during uterine contractions the intervillous space is distended. During uterine contraction more maternal blood is available for exchange with the fetal compartment.     

Histopathological study of placental bed biopsy in placenta previa

BACKGROUND: To study placental bed biopsy changes in placenta previa and normally implanted placenta. SUBJECT AND METHOD: Fifty placental bed biopsies from 50 patients with placenta previa and 50 placental bed biopsies from normally implanted placenta were taken at cesarean section. Placental bed biopsy was stained with hematoxyline and eosin for histological examination. Both the groups were compared for trophoblastic invasion and vascular changes of placental bed spiral arteries. Statistical analysis was done by Chi-square test. RESULTS: Placenta bed biopsy was representative in 42/50 (84%) biopsy samples of the study group (placenta previa) and 35/50 (70%) of the control group (normally located placenta). Trophoblastic giant cell migration into decidua was present in 100% of representative samples of both the groups while migration into myometrium was seen in 66.67% and 51.14% of samples of study and control group. Average number of trophoblastic giant cells per sample was significantly higher in placenta previa (decidua 41.3%, myometrium 52%) than the control group (decidua 17.4%; myometrium 14.5%). Trophoblastic giant cell infiltration into myometrial spiral arterioles was higher in placenta previa (81.83 cells per vessel). Percentage of myometrial spiral arterioles showing physiological changes was significantly higher in the study group (50.39%) compared to the control group (21.14%). Incidence of inflammatory cell infiltration was higher in the study group (42.86%). Hemorrhage into decidua and myometrium were seen in biopsy samples of the placenta previa. CONCLUSION: Placenta previa is associated with significantly higher trophoblastic giant cell infiltration and physiological changes of the myometrial spiral arterioles.     

Reactivities of the nongravid uterine vasculatures: Effects of norepinephrine

Responses of the component tissues of the nonpregnant ovine uterus to intravenous administration of norepinephrine were determined with radioactively labeled microspheres under flowmeter guidance. During a mean decrease in uterine conductance to 42 per cent of control, no significant differences in the distribution of uterine blood flow to caruncles, endometrium, myometrium, or cervix occurred. These observations differ from those during the last half of gestation, when placental vascular reactivity to norepinephrine is muted. They support the concept that fundamental changes in placental vascular responses occur during placentation.     

Uterine activity during the two hours after placental delivery among low-risk pregnancies: an observational study

Objective: The purpose of this study was to describe uterine activity within the first two hours after placental delivery among low-risk pregnant women.

Materials and methods: Participants were 17 low-risk pregnant women who had a singleton birth at midwifery birth centers in Japan. Contractile waves of uterine activity were measured by using an external tocodynamometer.

Results: Spontaneous uterine contraction frequency during the first two hours after the placental delivery decreased over time (F_9,?54?=_?19.7, p?<?0.001). The mean contraction intervals were 1.9?±?0.3?min, 2.4?±?0.9?min, 4.2?±?0.7?min and 7.9?±?2.1?min for the second stage, third stage, and the first hour and second hour after placental delivery, respectively. Uterine contraction frequency increased with oxytocin administration and infant suckling; however, an icepack to cool the uterus did not change the contraction waves. No correlations were found between uterine activity and blood loss or pain.

Conclusion: Contraction of the myometrium is the primary mechanism for hemostasis. The uterine contraction intervals became prolonged over time, and blood loss did not increase. The findings provide insight into the role of myometrium contraction as a hemostasis mechanism.     

Single cause for initiation of labor and toxemia: a hypothesis

A hypothesis is presented that states that the decline in oxygen tension (PO2) in the intervillous space causes both toxemia (preeclampsia-eclampsia) and the initiation of labor. The trophoblast is identified as the monitor of the fetal PO2 and as the source of substances that are released into the maternal circulation stimulating the myometrium, the heart, the vascular smooth muscle, and, perhaps, the brain. In the presence of normal trophoblast the release takes place only when the PO2 in the intervillous space decreases to a level at which the fetus should be expelled from the uterus to avoid intrapartum hypoxia. Near term, the myometrium is the most responsive site to the released substances, and stimulation of the heart and systemic vasculature is observed only infrequently. With release of these substances, intrapartum toxemia results. Toxemia before onset of labor is created by hypoxia of the trophoblast in the presence of a nonresponsive myometrium to materials released. A small placenta, compression of the intervillous space by villous edema, and avulsion of spiral arterioles are the main causes of the premature decline of intervillous space PO2, leading to toxemia. Postpartum toxemia is produced by the retained (extraplacental) trophoblast, perhaps facilitated by the rapid clearance of progesterone.     

Ritodrine infusion during late pregnancy: effects on fetal and placental blood flow, prostacyclin, and thromboxane

To study the effects of ritodrine on fetal and placental blood flow and maternal prostacyclin and thromboxane A2, 14 women with premature uterine contractions between the thirty-first and thirty-sixth weeks of pregnancy were treated with intravenous infusions of ritodrine, with incremental doses up to 200 micrograms per minute. The intervillous and the umbilical vein blood flows were measured before and after 1 hour of infusion of ritodrine, with the xenon 133 method and with a combination of real-time and Doppler ultrasonic equipment, respectively. Ritodrine decreased maternal diastolic and mean arterial pressures, as well as placental vascular resistance, but caused no significant changes in intervillous and umbilical vein blood flows. Ritodrine stimulated the synthesis of vasodilatory prostacyclin, as seen from a rise in maternal plasma 6-keto-prostaglandin F1 alpha, but inhibited the platelets' capacity to generate the vasoconstrictor thromboxane A2. Thus, apart from maternal hemodynamic changes, the intervillous and umbilical circulations are maintained during short-term administration of ritodrine in normotensive pregnancies.     

Radionuclide and angiographic studies of placental circulation in man and rhesus monkey

Imaging maternal and fetal circulation during perfusion of isolated human placental lobules was performed. Radionuclide and contrast angiograms, specimen scans, and histologic preparations obtained on human material during in vitro investigations were compared to the results obtained in vivo on pregnant rhesus monkeys. The distribution of maternal blood flow within the placenta appeared similar in both human and rhesus studies. The ‘spurts’ of radiopaque medium shown on the contrast angiograms correlated with the appearance of areas of increased radioactivity. These ‘hot spots’ are located where the uteroplacental spiral arteries open into the intervillous space or where the perfusion cannulae irrigate the maternal side of the placenta. Time-radioactivity curves reached an early peak and remained the same as did their distribution on delayed scans. The 15 to 30 μm microspheres injected into the intervillous spaces are not removed onto the venous side by maternal flow through arteriovenous communications (or ‘shunts’) but are retained in localized areas of the intervillous space adjacent to the spiral arteries. Many of these microspheres adhere to the ‘brush border’ of the chorionic villi syncytiotrophoblast. These comparative studies confirm that rhesus monkeys and perfused human placental lobules are relevant models to investigate uteroplacental hemodynamics.     

子宫肌瘤动脉血管网数字化三维模型构建与特点

目的 利用基于CT血管成像（CTA）三维重建技术构建的子宫肌瘤动脉血管网数字化三维模型，探讨子宫与子宫肌瘤的血管网特点。方法 连续采集2012年1月至9月于南方医科大学南方医院接受CTA检查的72例子宫肌瘤患者的原始数据集，构建子宫肌瘤动脉血管网数字化三维模型，通过逐步调整阈值以改变模型的血管显示密度，并予透明化处理后作分析。结果 成功构建了72例患者的子宫肌瘤动脉血管网数字化三维模型，该模型可清晰的显示子宫动脉及子宫肌层、子宫肌瘤的血管网，可见肌壁间、浆膜下、黏膜下子宫肌瘤的血管网轮廓与子宫血管网的相对位置不同，其中浆膜下肌瘤轮廓显示最为清晰。重建模型中存在特殊类型的肌瘤血管网。结论 利用CTA和重建软件构建出的子宫肌瘤动脉血管网数字化三维模型形态逼真，可准确识别子宫肌层与子宫肌瘤的血管网，为术前评估和临床教学提供参考。     

Effects of epinephrine on distribution of blood flow in the pregnant ewe.

Seven pregnant ewes ranging from 85 to 140 days of gestation were infused with systemic doses of epinephrine and uterine arterial flow dose-response curves were determined. With a constant systemic infusion of epinephrine at a mean rate of 0.29 +/- 0.03 mug/Kg.-min., and the radionuclide lebeled microsphere method to measure arterial blood flow, a 38.5 per cent decrease in total uterine arterial blood flow was demonstrated while systemic pressure was unaltered. At this dose the reduction in endometrial blood flow was significantly greater (-58.7 per cent) than that in either the myometrium (-36.9 per cent) or placental cotyledons (-34.5 per cent) (p less than 0.025 and less than 0.005, respectively). There also occurred a decrease in blood flow to the mammary gland and the pancreas, whereas increased in blood flow to the skeletal muscle, adipose tissue, and spleen were documented. It is evident from this study that during the period of ovine pregnancy investigated, the vascular bed of all tissues comprising the pregnant uterus, including the placental cotyledons, are sensitive to the vasoconstrictive effects of epinephrine.     

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants

An examination of the maternal vascular response to placentation shows that physiological changes in the placental bed normally extend from the decidua into the inner myometrium. In pre-eclampsia and in a proportion of pregnancies with small-for-gestational age infants (SGA) the physiological changes are restricted to the decidual segments alone. In addition, complete absence of physiological changes throughout the entire length of some spiral arteries is seen in pre-eclampsia and SGA. This new observation is confirmed in a study of basal plates of placentas from abnormal pregnancies. Intraluminal endovascular trophoblast may be seen in the placental bed spiral arteries in the third trimester in pre-eclampsia and SGA, a feature not seen beyond the second trimester in normal pregnancy. These findings point to a defect in the normal interaction between migratory trophoblast and maternal uterine tissues in pre-eclampsia and in SGA.     

Distribution of prostaglandin endoperoxide synthase and prostacyclin synthase in the late pregnant uterus

Prostacyclin (PGI2) synthase and prostaglandin endoperoxide synthase (cyclo-oxygenase; PGH synthase) were measured with specific immunoradiometric assays in myometrial microsomes from different areas of a primigravid uterus at 34 weeks gestation. PGH synthase concentrations increased significantly from fundus toward lower segment (P less than 0.005), but that trend did not apply to PGI2 synthase concentrations, which were significantly higher on the placental than on the non-placental side of the uterus (P less than 0.005). PGI2 synthase concentrations showed no further increase with increasing proximity to the placental bed. In myometrium underneath the placental bed there was an inverse relation between the PGH and PGI2 synthase concentrations (r = 0.86; P less than 0.01) which did not apply to other regions of the uterus. The data suggest that local rather than general mechanisms control uterine PGH and PGI2 synthase concentrations, and that uterine prostaglandin and PGI2 production strongly depend on anatomical relations that have been neglected in previous studies on uterine prostaglandin biosynthesis.     

Determination of the intervillous perfusion index in pregnancies with intrauterine growth retardation

The authors developed a new radioisotope technique to measure placental blood flow for early detection of placental insufficiency. Using this method placental perfusion has been measured in 20 healthy pregnant women and in 15 pregnancies complicated with intrauterine growth retardation (IUGR). The T-maximum pictures obtained made it possible to differentiate between the vascular and intervillous phases of placental blood flow. The time period of intervillous phase calculated as the percent of the whole placental T-maximum was given as the intervillous perfusion index (IPI). It has been demonstrated that IPI is significantly longer in IUGR pregnancies (67.0 +/- 14.6) than in the control group (31.6 +/- 10.7). These data suggest that the first sign of placental insufficiency is the prolongation of IPI, which is likely to precede the quantitative reduction of placental perfusion.     

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants

Summary. An examination of the maternal vascular response to placentation shows that physiological changes in the placental bed normally extend from the decidua into the inner myometrium. In pre-eclampsia and in a proportion of pregnancies with small-for-gestational age infants (SGA) the physiological changes are restricted to the decidual segments alone. In addition, complete absence of physiological changes throughout the entire length of some spiral arteries is seen in pre-eclampsia and SGA. This new observation is confirmed in a study of basal plates of placentas from abnormal pregnancies. Intraluminal endovascular trophoblast may be seen in the placental bed spiral arteries in the third trimester in pre-eclampsia and SGA, a feature not seen beyond the second trimester in normal pregnancy. These findings point to a defect in the normal interaction between migratory trophoblast and maternal uterine tissues in pre-eclampsia and in SGA.     

The pattern of interstitial trophoblasticinvasion of the myometrium in early human pregnancy

The human placental bed myometrium, studied in 42 intact hysterectomy specimens rangingfrom 8 to 18 weeks' gestation, is characterized by the presence of large numbers of non-villous invasive cytotrophoblastic cells. Quantitative morphometric analysis reveals a tendency for maximal invasive activity to occur at the centre and, subsequently, to extend centrifugally to produce an annular pattern. Morphological observations suggest that the intimate mixture of cytotrophoblast with myometrial tissue must affect the mechanical properties of the myometrium. Local hormone production by trophoblast may induce or enhance these and other changes in uterine tissues that are essential for the establishment of human placentation. Cytotrophoblastic invasion into the myometrium appears to be restricted to the earlier stages of gestation and morphological evidence indicates that, subsequently, clumps of cytotrophoblast fuse to form multinuclear syncytiotrophoblast, the characteristic placental bed giant cells.     

Deep placentation

Deep placentation in human pregnancy is realised by deep invasion of the placental bed by the extravillous trophoblast, involving the decidua and the inner (junctional zone) myometrium. Interstitial invasion of the stroma and endovascular trophoblast invasion of the spiral arteries both occur. Deep endovascular trophoblast invasion into the myometrial segments of spiral arteries is important for proper placental functioning. Before this extended vascular invasion begins, decidua-associated vascular remodelling, which includes swelling and disorganisation of the vascular smooth muscle, occurs during a period of rising placental oxygen. This early remodelling step may accommodate the progressively increasing maternal blood flow to the developing placenta. The subsequent trophoblast-associated remodelling step enhances and stabilises the widening of the vessels, whereas the vascular smooth muscle and elastic lamina are replaced by a fibrinoid matrix with embedded trophoblast. Defective deep remodelling contributes to placental malfunctioning in complications of pregnancy.     

The Comparison of Uterine Artery Doppler Velocimetry with the Histopathology of the Placental Bed

We determined the relationship between the histopathological findings of the placental bed and Doppler flow measurements of the uterine artery in women with preeclampsia and fetal growth retardation. Doppler velocimetry in the uterine artery was evaluated in 17 pregnant women with preeclampsia, 15 of whom had fetal growth retardation, and 20 normal pregnant women, within 14 days of Caesarean delivery and placental bed biopsy. The placental bed biopsies were evaluated in terms of trophoblast migration into the myometrium and physiological changes of the spiral arteries. The results were compared with Doppler velocimetry values. Trophoblast migration and physiological changes were not detected in 10 (59%) cases with preeclampsia and in 4 (20%) with normal pregnancies (p<0.05). In the preeclamptic group, 9 of 15 cases that were complicated with intrauterine growth retardation had no trophoblastic migration into the myometrium. The mean systolic/diastolic ratio, resistance index and pulsatility index of the uterine artery in women with preeclampsia and fetal growth retardation was significantly higher than women with normal pregnancies (p<0.01). The mean resistance index of the uterine artery in the impaired migration group was significantly higher than the migration group (p=0.02). The incidence of impaired trophoblast migration was significantly higher in the group with a high systolic/diastolic ratio (above 2.5) and resistance index (above 0.58) than cases with low systolic/diastolic ratio and resistance index (72%, 23% respectively, p<0.05). The incidence of early diastolic notch in the impaired trophoblast migration group was significantly higher than the migration group (57% versus 13%, p<0.01). Our study supports the hypothesis that high uterine artery flow resistance is related to the reduced trophoblast migration into the myometrium and inadequate physiological changes in the spiral arteries in women with intrauterine growth retardation and preeclampsia.