Embryological development of the heart

[gravenewworld]

What happens if the developing embyro and soon to be child is of a different blood type than the mother? At what point during development does the embryo start producing blood? The umbilical vein brings in oxygenated blood from the mother to the fetus' and also deoxygenated blood from the fetus to the placenta. Why do we not see an immune response in either the fetus or mother if they are of two different blood types?

 

[Evo]

What happens if the developing embyro and soon to be child is of a different blood type than the mother? At what point during development does the embryo start producing blood? The umbilical vein brings in oxygenated blood from the mother to the fetus' and also deoxygenated blood from the fetus to the placenta. Why do we not see an immune response in either the fetus or mother if they are of two different blood types?

We do find these problems.

Many pregnant women carry a fetus with a blood type different from their own, and the mother can form antibodies against fetal RBCs. Sometimes these maternal antibodies are IgG, a small immunoglobulin, which can cross the placenta and cause hemolysis of fetal RBCs, which in turn can lead to hemolytic disease of the newborn, an illness of low fetal blood counts that ranges from mild to severe.[3]

http://en.wikipedia.org/wiki/Blood_type

 

[bobze]

Clinically antibodies against ABO blood grouping don't really turn out to be a problem. You can test mothers who have had children with different blood groups and find the antibodies, some can be IgG (like evo points out IgG can cross the placenta) the amounts are generally minimal enough as to not cause a problem in the fetus.

Antibody response occurs in 2 phases, the primary response in which antigen presenting cells (APCs) select b-cells and allow them to proliferate. In a primary response there is a long lag phase and a lower concentration of antibodies made against the antigen. The secondary response is generally much faster and stronger, with a shorter lag phase.

In pregnancy (ie; if the mother has been "primed" by a fetus) this secondary response normally isn't large and the production of IgG antibodies resembles a primary response rather than a secondary.

There is an excellent reason for this as well. Innately, we have something called isohemagglutinins, which are native IgM antibodies against other blood groups--This is also the reason why we must match ABO blood groups for transfusions. There is enough isohemagglutinins present that in a blood transfusion they can cause massive lysis of said blood.

Here is an important part, IgM exists as rather large pentamers that do not cross the placenta. So even though isohemagglutinins exist in the mother against other ABO groups the major "defense" against those blood groups does NOT have access to the fetus. It is suspected the reason that IgG levels remain so low as well is because of this.

Rh factor on the other hand is a different story and more important one. http://en.wikipedia.org/wiki/Hemolytic_disease_of_the_newborn"

 

[bobze]

Sorry I guess I really only answered your last question there :) Let me address the others real fast as well.

At what point during development does the embryo start producing blood?

Erythropoiesis, the technical name for red blood cell (RBC) production starts early on in the fetus, primarily in the yolk sac. Around 3-4 weeks. This function moves to the liver and spleen around week 7 and stays there for the most part to around birth. As you get closer the birth the bone marrow starts to play a larger roll, where it will occur in adults.

The umbilical vein brings in oxygenated blood from the mother to the fetus' and also deoxygenated blood from the fetus to the placenta.

The mother's oxygenated blood doesn't actually come into contact with fetal blood (from a simplified view I guess, some fetal blood, particularly monocytes do escape into maternal circulation, but well let the histologists continue arguing about that) it fills small lacuna derived from invasive trophoblastic tissue (really neat tissue there by the way, its almost like controlled neoplastic cells!) and exchanges respiratory gasses and waste products across the placental membrane.

The umbilical vein attaches to the placenta and enters the body through the umbilical ring (soon to be your "belly button") and carries fetal oxygenated blood (not maternal blood) to the fetal liver. In the liver it links up with deoxygenated blood from the IVC (inferior vena cava) and is returned to the fetal heart (right atrium). Since in the fetus the oxygen isn't coming from the lungs, the blood is shunted from the right atrium to the left atrium via the foramen ovale (consequently what most people refer to when they say that the babies "heart wasn't closed" at birth, which resolves itself 99% of the time) and then out to the rest of the fetus. The blood ends up in the umbilical arteries (branches of the internal iliacs) and then back to the placental where it gets reoxygenated.

At birth the crimping of the umbilicus leads to reduced pressure in the venus side of fetal circulation and right side of the heart. This pressure decreases below the pressure of the atrial side and left side of the heart, which closes the foramen ovale redirecting blood flow from the right atrium to the right ventricle and through the pulmonary vasculature where the newborn's lungs will take over oxygenation.

 

[gravenewworld]

Wow, thanks all for the great info.