Critical care medicine · 2006
Graft protein C entrapment is associated with reduced phagocyte activation during reperfusion in human liver transplantation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Ilmakunnas Minna, Pesonen Eero J, Höckerstedt Krister, Mäkisalo Heikki, Fernandez Jose A, Griffin John H, Repo Heikki, Siitonen Sanna, Petäjä Jari
Аннотация
OBJECTIVE: To explore the potential anti-inflammatory role of protein C pathway in ischemia-reperfusion injury during liver transplantation.
DESIGN: Prospective, observational clinical study.
SETTING: Tertiary teaching hospital.
PATIENTS: Fifty adult patients undergoing liver transplantation for acute liver failure or chronic liver disease.
INTERVENTIONS: To assess changes occurring across the transplanted liver, samples of blood entering and leaving the graft were obtained simultaneously from portal and hepatic veins. Plasma protein C and activated protein C levels, neutrophil and monocyte CD11b and L-selectin expression, and leukocyte differential counts were measured. Postoperative liver function and outcome of transplantation were recorded.
MEASUREMENTS AND MAIN RESULTS: During reperfusion, protein C became entrapped within the graft (portal vein 49% [20-96%]; graft caval effluent 25% [12-76%], p < .001), without concomitant activated protein C outflow from the graft. Simultaneously, marked neutrophil and monocyte activation occurred within the graft. Enhanced hepatic protein C entrapment was associated with reduced neutrophil and monocyte activation (R = .377, p = .011; R = .389, p = .008, respectively) during reperfusion.
CONCLUSIONS: Protein C entrapment occurs immediately during reperfusion in the graft without concomitant activated protein C release, suggesting a shortage of activated protein C in the reperfused graft. The ongoing inflammatory response during reperfusion may lead to protein C and activated protein C utilization within the graft. Indeed, hepatic protein C entrapment is associated with reduced hepatic phagocyte activation, suggesting a regulatory role for protein C pathway in hepatic reperfusion in human liver transplantation.
DESIGN: Prospective, observational clinical study.
SETTING: Tertiary teaching hospital.
PATIENTS: Fifty adult patients undergoing liver transplantation for acute liver failure or chronic liver disease.
INTERVENTIONS: To assess changes occurring across the transplanted liver, samples of blood entering and leaving the graft were obtained simultaneously from portal and hepatic veins. Plasma protein C and activated protein C levels, neutrophil and monocyte CD11b and L-selectin expression, and leukocyte differential counts were measured. Postoperative liver function and outcome of transplantation were recorded.
MEASUREMENTS AND MAIN RESULTS: During reperfusion, protein C became entrapped within the graft (portal vein 49% [20-96%]; graft caval effluent 25% [12-76%], p < .001), without concomitant activated protein C outflow from the graft. Simultaneously, marked neutrophil and monocyte activation occurred within the graft. Enhanced hepatic protein C entrapment was associated with reduced neutrophil and monocyte activation (R = .377, p = .011; R = .389, p = .008, respectively) during reperfusion.
CONCLUSIONS: Protein C entrapment occurs immediately during reperfusion in the graft without concomitant activated protein C release, suggesting a shortage of activated protein C in the reperfused graft. The ongoing inflammatory response during reperfusion may lead to protein C and activated protein C utilization within the graft. Indeed, hepatic protein C entrapment is associated with reduced hepatic phagocyte activation, suggesting a regulatory role for protein C pathway in hepatic reperfusion in human liver transplantation.