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Desarrollo de insuficiencia cardíaca y defectos congénitos del tabique septal en ratones que carecen de óxido nítrico
Qingping Feng1, Wei Song, Xiangru Lu
1Department of Medicine, London Health Sciences Centre, London, Ontario, Canada. qfeng@uwo.ca
Circulation
|August 15, 2002
Resumen
La deficiencia endotelial de óxido nítrico sintasa (eNOS) conduce a un aumento de la mortalidad y defectos cardíacos congénitos, incluidos los defectos septal, en ratones. Esto está relacionado con un aumento de la apoptosis de los cardiomiocitos durante el desarrollo cardíaco.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- Biología del desarrollo Biología del desarrollo.
- Cardiología Molecular Cardiología Molecular
Sus antecedentes:
- La sintetasa de óxido nítrico endotelial (eNOS) es crucial para regular el crecimiento celular, la apoptosis y la perfusión tisular.
- Investigaciones anteriores indicaron que los ratones con deficiencia de eNOS exhiben válvulas bicúspidas aórticas anormales.
- El papel de eNOS en el desarrollo del corazón requiere más investigación.
Objetivo del estudio:
- Investigar el papel de eNOS en el desarrollo cardíaco.
- Evaluar el impacto de la deficiencia de eNOS en la función cardíaca y la supervivencia.
Principales métodos:
- Se examinó la mortalidad postnatal, la función cardíaca y los defectos del tabique septal en eNOS(-/-), eNOS(+/-) y ratones de tipo salvaje.
- Utilizó cristales de ultrasonido para medir el acortamiento del corazón.
- Se evaluó la apoptosis de los cardiomiocitos y la actividad de la caspasa-3 en las etapas embrionaria y neonatal.
Principales resultados:
- Aumento significativo de la mortalidad posnatal en ratones eNOS(-/-) (85,1%) y eNOS(+/-) (38,3%) en comparación con el tipo silvestre (13,3%).
- Se encontró congestión pulmonar severa y disminución del acortamiento cardíaco en ratones con deficiencia de eNOS.
- Se demostró un aumento significativo en los defectos del tabique auricular y ventricular en los neonatos eNOS(-/-) (75%) y eNOS(+/-) (32,4%) frente al tipo salvaje (4,9%).
- Se observó un aumento de la apoptosis de los cardiomiocitos y la actividad de la caspasa-3 en los embriones y neonatos eNOS.
Conclusiones:
- La deficiencia de eNOS resulta en insuficiencia cardíaca y defectos septos congénitos durante el desarrollo cardíaco.
- El aumento de la apoptosis de los cardiomiocitos se asocia con la deficiencia de eNOS y anomalías cardíacas.
- eNOS es esencial para el desarrollo normal del corazón.
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