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ABSTRACT
The transfer of O2 from the maternal to prenatal circulation is facilitated by higher O2 affinities in prenatal blood. The affinity shifts that may compensate for lack or feeble development of placental connections result from different operating conditions for the Hb (such as lower concentrations of organic phosphates that depress Hb-O2 affinity in the fetal red cells), or the occurrence of specific fetal and embryonic Hb's that have either higher intrinsic O2 affinities than adult Hb or lower sensitivities to phosphate cofactors. The affinity shifts correlate with amino acid substitutions at very few, key positions in the Hb protein moieties and thus demonstrate conservatism in molecular strategies. The complex molecular systems encountered in early embryos may favor homeostasis in tissue O2 supply and compensate for their lower organization at the organ level compared to adults.