Biosíntesis de tromboxano A2 y prostaciclina en niños y adolescentes con enfermedad vascular pulmonar
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I Adatia1, S E Barrow, P D Stratton
1Developmental Vascular Biology and Pharmacology Unit, United Medical School, Guy's Hospital, London, UK.
Circulation
|November 1, 1993
Resumen
Los niños con enfermedad cardíaca congénita muestran un aumento de la biosíntesis de tromboxano (TX) A2, lo que indica un desequilibrio con la prostaciclina (PGI2). Este desequilibrio puede impulsar la progresión de la enfermedad vascular pulmonar y persiste incluso en pacientes mayores.
Área de la Ciencia:
- Cardiología Pediátrica Cardiología pediátrica.
- La hipertensión pulmonar es la hipertensión pulmonar.
- Biología Vascular Biología Vascular
Sus antecedentes:
- La patogénesis de la enfermedad cardíaca congénita (CHD) en los niños no se entiende completamente.
- El tromboxano (TX) A2 y la prostaciclina (PGI2) tienen funciones opuestas en la función vascular.
- Un desequilibrio en la biosíntesis de TXA2 y PGI2 puede contribuir a la resistencia vascular pulmonar y la trombosis en la ECH.
Objetivo del estudio:
- Investigar la biosíntesis de TXA2 y PGI2 en niños con ECC.
- Para determinar si un desequilibrio en estos eicosanoides contribuye a la enfermedad vascular pulmonar.
- Para evaluar los cambios en los metabolitos TXA2 y PGI2 después de la corrección quirúrgica de CHD.
Principales métodos:
- Se midió la excreción urinaria de 2,3-dinor-TXB2 y 2,3-dinor-6-oxo-PGF1 alfa en niños pequeños con ECC y controles sanos.
- Comparación de la excreción de metabolitos en pacientes con enfermedad vascular pulmonar reversible versus irreversible.
- Cambios evaluados en la excreción de metabolitos después de la cirugía cardíaca.
Principales resultados:
- Los niños con ECC y aumento del flujo sanguíneo pulmonar tenían una excreción de 2,3-dinor-TXB2 significativamente mayor que los controles.
- La excreción de 2,3-dinor-6-oxo-PGF1 alfa fue similar entre pacientes y controles.
- Después de la cirugía, la excreción de 2,3-dinor-TXB2 disminuyó en los pacientes, acercándose a los niveles de control.
- Los pacientes con enfermedad vascular pulmonar avanzada mostraron una mayor proporción de metabolito TXA2 a PGI2.
Conclusiones:
- El aumento de la excreción de 2,3-dinor-TXB2 en niños con ECC sugiere un desequilibrio en la biosíntesis vascular pulmonar de TXA2 y PGI2.
- Este desequilibrio puede impulsar la progresión de la resistencia vascular pulmonar en la enfermedad coronaria.
- El desequilibrio persiste en pacientes de ECC mayores y no corregidos, lo que contribuye a la progresión de la enfermedad.
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