El sistema vasodilatador óxido nítrico sintasa endotelial (eNOS) en pulmón de fetos sometidos a hipoxia crónica

Autores/as

  • Daniel Miranda S. Alumno Escuela de Medicina, Universidad de Chile
  • María Mazzoni W. Alumna Escuela de Medicina, Universidad de Chile
  • Valeria Martínez A. Alumna Escuela de Medicina, Universidad de Chile
  • Rodrigo Montecinos M. Alumno Escuela de Medicina, Universidad de Chile
  • Víctor Reyes C. Programa de Fisiopatología, ICBM, Facultad de Medicina, Universidad de Chile.
  • Germán Ebensperger D. Programa de Fisiopatología, ICBM, Facultad de Medicina, Universidad de Chile.

Resumen

Introducción: Al nacimiento, la circulación pulmonar pasa de un estado de alta a uno de baja resistencia, lo que implica el establecimiento de un nuevo balance entre vasoconstrictores y vasodilatadores. Un importante vasodilatador es NO, el que puede ser producido por la enzima eNOS. La falla de esta transición provoca un cuadro clínico llamado hipertensión pulmonar persistente, una de sus causas es hipoxia fetal crónica, observada en gestaciones a grandes altitudes. Se investigó si produce disminución de la expresión de eNOS en el pulmón.

Metodología: El estudio se realizó en fetos de oveja de 80 % de gestación, gestados a 520 o a 3600 m.s.n.m. Se midió la expresión de eNOS en extractos proteicos de pulmón mediante inmunoblot.

Resultados: No se observó diferencia significativa entre ambos grupos.

Conclusiones: La hipoxia crónica no produce cambios significativos sobre la expresión de eNOS en el pulmón de fetos de oveja a esta edad gestacional.

Palabras clave:

hipoxia fetal, hipertensión pulmonar, óxido nítrico sintasa

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