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Circulación hiperdinámica en la cirrosis: ¿un papel para el óxido nítrico?
1Wellcome Research Laboratories, Langley Court, Beckenham, Kent, UK.
Lancet (London, England)
|March 30, 1991
Resumen
La cirrosis causa hipotensión debido al aumento de la producción de óxido nítrico (NO). Este potente vasodilatador, el óxido nítrico, conduce a una baja resistencia vascular y una menor sensibilidad a los vasoconstrictores en pacientes con enfermedad hepática.
Área de la Ciencia:
- Fisiología cardiovascular fisiología cardiovascular.
- Hepatología Hepatología.
- Biología Vascular Biología Vascular
Sus antecedentes:
- La cirrosis se caracteriza por hipotensión, baja resistencia vascular sistémica y disminución de la sensibilidad vasoconstrictora.
- Estas alteraciones hemodinámicas pueden deberse a una sobreproducción de vasodilatadores.
- El óxido nítrico (NO) es un vasodilatador clave sintetizado y liberado por los vasos sanguíneos periféricos.
Objetivo del estudio:
- Para investigar el papel del óxido nítrico (NO) en los cambios cardiovasculares asociados con la cirrosis.
- Explorar el vínculo potencial entre la endotoxemia en la cirrosis y la inducción sostenida de la NO sintasa.
Principales métodos:
- Revisión de los estudios en animales existentes sobre la expresión de la NO sintasa inducida por endotoxinas y citoquinas.
- Análisis de los efectos fisiológicos de la liberación sostenida de NO en el tono vascular.
- Correlación de la prevalencia de endotoxemia en la cirrosis con los cambios hemodinámicos observados.
Principales resultados:
- Los estudios en animales demuestran que las endotoxinas y citoquinas bacterianas inducen la NO sintasa, lo que lleva a la liberación sostenida de NO y a la hipotensión.
- La endotoxemia es una complicación frecuente en pacientes con cirrosis.
- Se supone que la inducción persistente de la NO sintasa subyace al perfil hemodinámico característico de la cirrosis.
Conclusiones:
- El aumento de la síntesis y liberación de óxido nítrico (NO) probablemente contribuya significativamente a la hipotensión y a la baja resistencia vascular sistémica observada en la cirrosis.
- La inducción persistente de la NO sintasa, potencialmente desencadenada por la endotoxemia común en la cirrosis, puede explicar estos cambios hemodinámicos sostenidos.
- Dirigirse a las vías de producción de NO podría ofrecer estrategias terapéuticas para el manejo de la disfunción cardiovascular en la enfermedad hepática.
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