Abstract
One of the most common insults during early stages of postnatal ontogenetic development is hypoxemia due to cyanotic congenital heart defects. The question of the presumed cardiac impact will be, therefore, of considerable importance.
Experimental results have clearly shown that the immature heart is significantly more tolerant to acute oxygen deficiency than the adult myocardium. However, the mechanisms of this difference have not yet been satisfactorily clarified; they are likely the result of developmental changes in cardiac mitochondrial function and energy metabolism.
Adaptation to chronic hypoxia confers long-lasting protection in both adult and immature heart. However, the already high resistance of the newborn heart cannot be further increased; the effects of protective mechanisms appear only when the ischemic tolerance starts to decrease during development.
Early chronic hypoxia, although transient, may have serious sex-dependent late consequences on the adult cardiovascular system. These results support the view that precise knowledge of individual developmental periods that are critical for cardiac ontogeny is crucial for better understanding of the mechanism of cardiac adaptation to oxygen deficiency.