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a Chapter 16 Doppler Velocimetry of the Uteroplacental Circulation 229<br />

Fig. 16.3. Fully developed physiologic<br />

changes in the uteoplacental arteries<br />

during normal pregnancy. Hatched portions<br />

of the wall of these vessels indicate<br />

the extent of the physiologic<br />

changes. I. V. S. intrvillous space. (From<br />

[113] with permission)<br />

changes. In all, approximately 100±150 converted<br />

spiral arteries supply the placental bed. It is believed<br />

that these uteroplacental vessels have lost their ability<br />

to respond to vasoactive substances.<br />

The question arises whether this change from<br />

small muscular arteries to dilated tortuous vessels is<br />

entirely responsible for the increase in flow from<br />

100 ml/min to 500±800 ml/min. All large vessels of<br />

the pregnant uterus, regardless of whether they supply<br />

the placental bed, undergo hyperplasia and hypertrophy<br />

[17]. Thus the increase in cross-sectional<br />

area leads to a reduction in resistance and further development<br />

of the uterine circulation. This increase in<br />

luminal diameter of the large vessels probably accounts<br />

for the increase in uteroplacental flow during<br />

the third trimester. In addition, the effects of the hormones<br />

estrogen and progesterone, the increased<br />

blood volume and cardiac output, the diminished<br />

blood viscosity, and the lowered peripheral resistance<br />

influence uterine flow.<br />

Abnormal Development<br />

of the Uteroplacental Circulation<br />

in the Presence of Essential<br />

Hypertension, Preeclampsia,<br />

and Intrauterine Growth Restriction<br />

According to Brosens et al. [15], Robertson et al.<br />

[16], and Khong et al. [18], a lack of endovascular infiltration<br />

by trophoblasts into the myometrial portion<br />

of the placental bed spiral arteries is a consistent<br />

finding in the presence of preeclampsia. The physiologic<br />

changes of the placental bed spiral arteries<br />

extend only to the deciduomyometrial junction<br />

(Fig. 16.4). With preeclampsia the spiral arteries may<br />

remain unconverted throughout their decidual and<br />

myometrial length (Fig. 16.5). Thus there is both an<br />

incompleteness in the degree of endovascular trophoblastic<br />

invasion of the spiral arteries, being confined<br />

to the decidual portion, and a reduction in the number<br />

of uteroplacental arteries formed. The diameter of<br />

the spiral arteries remains at 200±300 lm. Sheppard<br />

and Bonnar [19] reported the picture not to be so<br />

clear-cut, as they observed physiologic changes in the<br />

myometrial spiral arteries in preeclamptic pregnan-<br />

Fig. 16.4. Difference between normal<br />

and preeclamptic pregnancies regarding<br />

the extent of physiologic changes<br />

in the uteroplacental arteries. With<br />

preeclampsia these changes do not<br />

extent beyond the deciduomyometrial<br />

junction. (From [113] with permission)

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