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In the plasma of chicken embryo increasing concentration of the catecholamines protects the embryo against hypoxic damages via improvement of the blood gas status (β-adrenergic receptors and increasing of the metabolites of glycolysis). In addition, there is an increasing number of capillaries.
Consequently, the rate of gene expression of the hypoxia inducible genes should be measured as an indicator of an adaptation of the embryonic heart to the oxygen deficiency.
From day (D) 6 -12 the eggs were incubated under chronic hypoxic conditions with 12%O2 in the incubation air.
Heart withdrawals were carried out at D12 and D18. At the D 18 another two groups of the embryo were exposed to an acute oxygen deficiency again, 0% O2 for 30 or 45 min.
The rate of expression of the enzyme of glycolysis , Enolase and the endothelial growth factor (VEGF) were determined in the heart cells by means of quantitative PCR (real- time PCR).
1. At D12 the gene expression of Enolase and VEGF were overexpressed in the hearts which were incubated from D6 to D12 less than 15% O2.
2. No overexpression has to be measured after further 6 days incubation at 21% O2 3. Acute O2 deficiency has no influence.
In the middle third of the incubation (D6-D12) the embryonic heart muscle cells are affected by chronic hypoxia. Acute hypoxic stress did not show any influence. The gene expression seems to be effected by chronic hypoxia. Cells react in two distinguished ways: 1. Heart muscle cells produce alterations of the aerobic to the anaerobic metabolism and activate the glycolytic metabolism. In this case the cells produce energy. 2. Exposure to chronic prenatal hypoxia results in an adaptation of the endothelial growth factor (VEGF) and this leads to an improvement of O2 –concentration in the embryonic heart via increasing number of the capillaries.