Carrillo-Esper R, Villaseñor-Ovies P

Idioma: Español
Referencias bibliográficas: 59
Paginas: 219-230
Archivo PDF: 145.78 Kb.

RESUMEN

La coagulación consiste en una serie de reacciones que se generan en la superficie celular y cuyo objetivo es la formación de trombina en sitios de lesión vascular. El modelo tradicional de la coagulación, propuesto hace 40 años, separa las fases celular y humoral de la coagulación y considera que el proceso de hemostasia se consigue a través de la activación secuencial de enzimas efectoras en dos vías independientes. Recientemente se desarrolló un nuevo modelo que ha permitido un mejor entendimiento de cómo el sistema de hemostasia funciona in vivo. Esta nueva teoría, conocida como modelo celular de la coagulación enfatiza la interacción entre los factores solubles y las superficies celulares y considera a las células como elementos esenciales capaces de dirigir el proceso hemostático. En el nuevo modelo, la coagulación se sucede en tres fases que ocurren en distintas superficies celulares y de manera simultánea: iniciación, amplificación y propagación y resalta la importancia del complejo factor VII/factor tisular en la fase de activación del sistema. Este nuevo modelo generó las bases para el uso terapéutico de altas dosis de factor VII recombinante activado en pacientes con hemorragia debida a anormalidades en la hemostasia en distintas entidades clínicas que incluyen la coagulopatía del paciente quirúrgico. El objetivo de esta revisión es analizar el nuevo modelo celular de la coagulación y su impacto en las opciones terapéuticas del paciente quirúrgico con hemorragia.

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