The thick muscular walls of the umbilical vessels respond to various stimuli such as trauma, tension, sympathomimetic amines, bradykinin, angiotensin, and changes in PO2. In animals without a tied umbilical cord, hemorrhage in newborns is minimized by the constriction of these large umbilical vessels when the umbilical arteries stretch and there is an increase in PO2 in systemic arteries.

When blood flow through the umbilical vein stops, the ductus venosus, a vessel with a muscular sphincter, closes. However, the factor that triggers the closure of the ductus venosus remains unknown.

In cases of hypoxia in pregnant women, the reduced blood PO2 in the fetus leads to tachycardia and an increase in blood flow through the umbilical vessels. If the hypoxia persists or if the flow through the umbilical vessels is impaired, fetal distress occurs, which initially presents as bradycardia.

A schematic diagram of the fetal circulation (Fig. 17.44) shows the percentages of O2 saturation in different blood vessels. The blood leaving the placenta is 80% saturated, but when it passes through the foramen ovale, its saturation is reduced to 67%. This reduction occurs due to the mixing of saturated blood with desaturated blood from the lower part of the fetal body and the liver. The addition of desaturated blood from the fetal lungs further reduces the O2 saturation of left ventricular blood to 62%, which is the saturation level of the blood reaching the fetal head and upper extremities. The blood in the right ventricle, which is a mixture of desaturated superior vena cava blood, coronary venous blood, and inferior vena cava blood, is only 52% saturated with O2. When the major portion of this blood travels through the ductus arteriosus and joins the blood pumped by the left ventricle, the resulting O2 saturation of the blood traveling to the lower part of the fetal body and back to the placenta is 58%. An inset at the upper left of the diagram illustrates the direction of flow of a major portion of the inferior vena cava blood through the foramen ovale to the left atrium. Arrows indicate the directions of flow.

Immediately after birth, the asphyxia caused by the constriction or clamping of the umbilical vessels, along with body cooling, activates the respiratory center in newborn infants. As the lungs fill with air, pulmonary vascular resistance decreases to about 10% of its pre-lung expansion value. This reduction in vascular resistance is not due to the presence of O2 in the lungs since the change is the same even if the lungs are filled with N2. However, filling the lungs with liquid does not decrease pulmonary vascular resistance.

After birth, the left atrial pressure is elevated above that in the inferior vena cava and right atrium due to several factors: (1) the decrease in pulmonary resistance, resulting in a large blood flow through the lungs to the left atrium; (2) the reduction in flow to the right atrium caused by the closure of the umbilical vein; and (3) the increased resistance to left ventricular output caused by the closure of the umbilical arteries. The reversal of the pressure gradient across the atria leads to the abrupt closure of the valve over the foramen ovale, and over several days, the septal leaflets fuse together.
The umbilical vessels have thick muscular walls that react to trauma, tension, sympathomimetic amines, bradykinin, angiotensin, and changes in PO2. In animals in which the umbilical cord is not tied, hemorrhage of the newborn is minimized by constriction of these large umbilical vessels in response to stretching of the umbilical arteries and by an associated increase in PO2 in systemic arteries.
Closure of the umbilical vessels increases total peripheral resistance and the arterial blood pressure of the infant. When blood flow through the umbilical vein ceases, the ductus venosus, a thick-walled vessel with a muscular sphincter, closes. The factor that initiates closure of the ductus venosus is unknown.
Ifapregnantwomanissubjectedtohypoxia,thereducedbloodPO2inthefetusevokestachycardiaandanincreaseinbloodflowthroughtheumbilicalvessels.Ifthehypoxiapersistsorifflowthroughtheumbilicalvesselsisimpaired,fetaldistressoccursandismanifestedinitiallyasbradycardia.
•Fig. 17.44 Schematic Diagram of the Fetal Circulation. Thenumbers representthepercentageofO2saturationofthebloodflowingintheindicatedbloodvessel.Fetalbloodthatleavestheplacentais80%saturated,butthesaturationofthebloodthatpassesthroughtheforamenovaleisreducedto67%.ThisreductioninO2saturationiscausedbythemixingofsaturatedbloodwithdesaturatedbloodreturningfromthelowerpartofthefetalbodyandtheliver.AdditionofthedesaturatedbloodfromthefetallungsreducestheO2saturationofleftventricularbloodto62%,whichisthelevelofsaturationofthebloodreachingthefetalheadandupperextremities.Thebloodintherightventricle—whichisamixtureofdesaturatedsuperiorvenacavalblood,coronaryvenousblood,andinferiorvenacavalblood—isonly52%saturatedwithO2.Whenthemajorportionofthisbloodtraversestheductusarteriosusandjoinsthatpumpedbytheleftventricle,theresultingO2saturationofthebloodtravelingtothelowerpartofthefetalbodyandbacktotheplacentais58%.Theinset atupperleftillustratesthedirectionofflowofamajorportionoftheinferiorvenacavalbloodthroughtheforamenovaletotheleftatrium.Arrows indicatethedirectionsofflow.(DatafromDawesGS,etal.J Physiol. 1954;126:563.)
Immediately after birth, the asphyxia caused by constriction or clamping of the umbilical vessels, together with cooling of the body, activates the respiratory center of the newborn infant. As the lungs fill with air, pulmonary vascular resistance decreases to approximately 10% of the value that existed before lung expansion. This change in vascular resistance is not caused by the presence of O2 in the lungs because the change is just as great if the lungs are filled with N2. However, filling the lungs with liquid does not reduce pulmonary vascular resistance.
After birth, left atrial pressure is raised above that in the inferior vena cava and right atrium by (1) the decrease in pulmonary resistance, with the consequent large flow of blood through the lungs to the left atrium; (2) the reduction of flow to the right atrium caused by occlusion of the umbilical vein; and (3) the increased resistance to left ventricular output produced by occlusion of the umbilical arteries. Reversal of the pressure gradient across the atria abruptly closes the valve over the foramen ovale, and the septal leaflets fuse over a period of several days.