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Development of the ectopia cordis induced by hydrocortisone administration
V Seichert1, L Heringová, A Seichertová
1Institute of Anatomy, 1st Faculty of Medicine, Charles University, Prague, Czech Republic.
Folia Biologica
|March 24, 2000
Summary
Hydrocortisone treatment in chick embryos caused ectopia cordis (EC), a heart development defect. This suggests that membrana reuniens integrity is not essential for EC, but rather reduced mesenchyme proliferation is key.
Area of Science:
- Developmental biology
- Embryology
- Teratology
Background:
- Previous research linked mechanical disturbance of the membrana reuniens to ectopia cordis (EC) in chick embryos.
- The essential role of membrana reuniens integrity in EC development remained unclear.
Purpose of the Study:
- To investigate whether membrana reuniens disturbance is essential for EC development.
- To elucidate the mechanism underlying hydrocortisone-induced EC.
Main Methods:
- Intraamniotic administration of hydrocortisone on the 4th embryonic day in chick embryos.
- Histological examination of the membrana reuniens in embryos with EC.
- Flow cytometry analysis of cell cycle proliferation in prospective body-wall mesenchyme.
Main Results:
- Hydrocortisone induced EC in 84.8% of embryos.
- The membrana reuniens remained continuous, though thin, during EC development.
- Hydrocortisone-induced EC was associated with significantly reduced proliferation of anterior thoracic wall mesenchyme.
Conclusions:
- Membrana reuniens integrity is not essential for EC development.
- Reduced proliferation of prospective body-wall mesenchyme is a probable mechanism for hydrocortisone-induced EC.
- This study provides insights into the teratogenic effects of hydrocortisone on heart development.