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2008, Número 4

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Cir Cir 2008; 76 (4)


Donador exógeno de óxido nítrico en la respuesta inflamatoria hepática y hemodinámica después de choque hemorrágico

Anaya-Prado R, Toledo-Pereyra LH, Ren-Feng G, Reuben J, Ward PA

Idioma: Español
Referencias bibliográficas: 31
Paginas: 291-298
Archivo PDF: 121.71 Kb.


RESUMEN

Introducción: El choque hemorrágico resulta en estrés oxidativo celular e inducción de respuesta inflamatoria. Investigamos la capacidad del nitroprusiato de sodio para reducir la lesión tisular en un modelo animal de choque hemorrágico no controlado.
Material y métodos: 72 ratas Sprague-Dawley distribuidas en cuatro grupos: sham/salina, sham/nitroprusiato de sodio, choque/salina, choque/nitroprusiato de sodio. Se provocó choque hemorrágico (3 ml/100 g) en un periodo de 15 minutos; corte de cola y administración de la droga a los 30 minutos; reanimación hídrica con solución de ringer lactado (RL) para alcanzar presión arterial media (PAM) de 40 mm Hg; una fase de 60 minutos con hemostasia y reanimación hídrica con solución de RL para mantener PAM de 70 mm Hg; y una fase de observación de tres días. El tratamiento al inicio de la reanimación consistió en solución salina o 0.5 mg/kg de nitroprusiato de sodio. Se evaluó requerimiento hídrico para reanimación, función hepática, mieloperoxidasa de tejido hepático, histología hepática y sobrevida.
Resultados: El nitroprusiato de sodio redujo significativamente los requerimientos hídricos para reanimación (p = 0.0001) y produjo mejoría en las pruebas de lesión hepática, infiltración neutrofílica evidenciada por mieloperoxidasa de tejido hepático, y estudios histológicos. Se incrementó la sobrevida de 40 % en los controles a 60 % con el nitroprusiato de sodio.
Conclusiones: El exceso de óxido nítrico media la lesión hepática inducida por el choque hemorrágico, y la supresión de óxido nítrico con nitroprusiato de sodio puede reducir las consecuencias patológicas de la hemorragia severa, posiblemente por la eliminación del anión superóxido (O2–), limitando la producción de radicales más tóxicos.


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