The fetus as we have seen is totally dependent on oxygen from its mother’s lungs. This oxygen travels around the mother’s bloodstream attached to the hemoglobin molecules of the erythrocytes, arrives at the placenta, diffuses across into the fetal bloodstream and finally reaches the fetus at a much lower oxygen pressure than in the maternal blood. This reduced oxygen pressure is about the same as that on the top of Mount Everest, certainly not enough for an adult.
The fetus, however, copes with this low pressure in several ways. First of all its heart beats extremely fast, about 150 times per minute, compared to an average adult rate of only seventy to eighty times. This ensures a swift movement of fetal red blood cells to pick up placental oxygen (it takes only thirty seconds to make a complete fetal round trip.)
The fetus has more red blood cells per cubic millimeter than an adult (seven million/mm
compared to an average adult value of five million/mm
Fetal red blood cells also have a greater affinity for oxygen at a lower oxygen pressure than adult red blood cells.
Fetal erythrocytes are larger (8.3 microns) as compared to adult cells (7.5 microns) and thus each fetal cell can carry more oxygen.
Hemoglobin F (fetal) is found in most red blood cells before birth while hemoglobin A (adult) predominates after, but it is not clear that HbF has a greater affinity for oxygen than HbA.
The formation of red blood cells and different kinds of hemoglobin in the embryo and fetus is fascinating. The first site of red blood cell formation is the embryonic yolk sac at about three weeks (see photos in Nilsson, 1977). This organ disappears before three months but meanwhile the embryonic liver is making red blood cells (from thirty-five days and well into pregnancy). The final fetal site is the bone marrow which starts erythrocyte production at about the third to fourth month of pregnancy and continues throughout our adult lives.
At birth, the marrow of all our bones is making blood cells but in adults, only the vertebrae, ribs, sternum, part of the skull and the proximal ends of the humerus and femur are still engaged in red blood cell production (Crelin, 1973).
Three different hemoglobins are produced by the unborn child, with one switching off as the next one starts production. The different hemoglobins all contain the same heme molecules with an iron atom in the center but they all have different globins (amino acid chains) designated by Greek letters.
For the first eight weeks of prenatal life most of the hemoglobin is of the type called embryonic hemoglobin (HbE). Production of this is soon ended and fetal hemoglobin (HbF) becomes the single most important hemoglobin. At thirty-five weeks , ninety percent of the fetal cells still contain HbF but it is starting to decrease and the amount of HbA (adult hemoglobin) begins to increase. At birth the production of HbF is almost totally switched off, so that in a normal year-old child only two percent of the red blood cells contain HbF while the great majority contain only HbA. This switching on and off of hemoglobin production is under the control of certain regulatory genes. Occasionally something goes wrong and an adult never develops any HbA-his red blood cells contain only fetal hemoglobin. Luckily he can lead a completely normal life (Singer and Hilgard, 1978).
protect individuals in certain cases. If an infant has been born with sickle cell anemia (two genes for hemoglobin S) it will not show any symptoms for the first six months of its life, as long as there is still some HbF in its blood to protect it.