Background
Proliferation and differentiation are the two main regulators for the cell growth. During the period of proliferation and maturation, oxygen plays a vital role. The fetus responds to chronic hypoxia by increasing its cardiac output by 50% than the normal. Chronic hypoxic expo-sure during development can produce impact in both anatomical and physiological ontogeny. When exposed to hypoxic conditions chicken embryos develop relatively larger hearts than under normal conditions.
Previous studies suggest that lower oxygen tension in the fetus is essential for normal heart formation. However, physiologically, hypoxia will lead to adverse effects which lead to changes in structure, function and gene expression in fetal hearts. Although fetal hearts have a remarkable ability to grow under low oxygen condition, chronically induced hypoxia imposes short and long term complications like vasculogenesis, angiogenesis, chondrogenesis and fetal heart remodelling (Ascuitto et al., 1996).
Studies in chickens to understand the hemodynamic changes (mean arterial pressure, heart rate and peripheral arterial resistance) during fetal development under hypoxic conditions and transition of cardiomyocytes from hyperplasia to hypertrophy during postnatal development have been extensively made (Faqian et al., 1997). The effects of cardiovascular changes during fetal development under hypoxic condition are poorly understood
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Director of undergraduate studies Biology
Last updated:
05/20/12