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Aumento de la biosíntesis de tromboxano en la hipercolesterolemia tipo IIa.

G Davì1, M Averna, I Catalano

  • 1Department of Medicine, University of Palermo School of Medicine, Italy.

Circulation
|May 1, 1992
PubMed
Resumen
Este resumen es generado por máquina.

La biosíntesis de tromboxano plaquetario A2 (TXA2) está elevada en la hipercolesterolemia tipo IIa, vinculada al colesterol alto. La aspirina en dosis bajas reduce efectivamente la excreción del metabolito TXA2, lo que indica una activación plaquetaria dependiente de TXA2.

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Área de la Ciencia:

  • Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular
  • La bioquímica es la bioquímica.
  • Farmacología Farmacología.

Sus antecedentes:

  • Se ha informado que la producción de tromboxano A2 (TXA2) en las plaquetas está aumentada en la hipercolesterolemia tipo IIa.
  • Este estudio investiga la relevancia in vivo de la producción de TXA2 mediante la medición de los metabolitos urinarios.

Objetivo del estudio:

  • Para evaluar in vivo la biosíntesis del tromboxano A2 (TXA2) en la hipercolesterolemia tipo IIa.
  • Para correlacionar la excreción del metabolito TXA2 con los niveles de colesterol y la función plaquetaria.
  • Evaluar el efecto de la simvastatina y la aspirina en la producción de TXA2.

Principales métodos:

  • Se midieron 11-dehidro-TXB2 y 2,3-dinor-TXB2 urinarios en 46 pacientes con hipercolesterolemia y 20 controles utilizando ensayos radioinmunológicos.
  • La excreción de metabolitos correlacionada con los umbrales de agregación de colágeno/araquidonato, la producción de plaquetas TXB2 in vitro y el colesterol plasmático.
  • Efectos evaluados de la simvastatina y la aspirina en dosis bajas sobre los metabolitos urinarios de TXA2.

Principales resultados:

  • La excreción urinaria de 11-dehidro-TXB2 fue significativamente mayor en los pacientes (68,7 ng / h) frente a los controles (22,4 ng / h), con el 74% de los pacientes que superaron los niveles normales.
  • La excreción se correlaciona con la sensibilidad a la agregación plaquetaria, la producción in vitro de TXB2 y el colesterol total en plasma.
  • La simvastatina redujo el colesterol y los metabolitos de TXA2, pero las reducciones no se correlacionaron.
  • La dosis baja de aspirina inhibió la excreción de 11-dehidro-TXB2 en aproximadamente un 70%.

Conclusiones:

  • La biosíntesis mejorada de TXA2 ocurre en la mayoría de los pacientes con hipercolesterolemia tipo IIa.
  • La producción elevada de TXA2 se debe en parte a niveles anormales de colesterol.
  • La aspirina en dosis bajas suprime eficazmente el aumento de la excreción del metabolito TXA2, lo que confirma la activación plaquetaria dependiente de TXA2 in vivo.