[Preacondicionamiento isquémico remoto sobre viabilidad del injerto hepático]. / Remote ischemic preconditioning in liver graft viability.

ANTECEDENTES: El preacondicionamiento isquémico remoto (PIR) en trasplante hepático ha sido sugerido en el ámbito experimental como estrategia para disminuir la lesión por isquemia- reperfusión. OBJETIVO: Evaluar el efecto del PIR sobre el injerto hepático en donante cadáver y el impacto de diversos mediadores inflamatorios en este proceso. MÉTODO: Se incluyeron 10 receptores de trasplante hepático, 5 controles y 5 con PIR, el cual fue realizado en los donantes cadavéricos mediante la aplicación de un torniquete neumático en ambos muslos por 10 minutos seguido de 10 minutos de reperfusión. Se determinaron interleucina (IL)-1, IL-6, factor de necrosis tumoral alfa (FNT-α), factor de crecimiento endotelial vascular (FCEV) y molécula de adhesión intracelular (ICAM)-1, parámetros hematológicos y bioquímicos en diversas fases del trasplante hepático. RESULTADOS: Se observó un aumento significativo de la aspartato aminotransferasa (AST), la alanino aminotransferasa (ALT) y la fosfatasa alcalina en las fases tempranas tras el trasplante hepático, y a las 72 horas los sujetos con PIR mostraron mejor respuesta, con recuperación de plaquetas, que persistió hasta los 3 meses en este grupo. La IL-6 participa en las fases tempranas de la lesión por isquemia- reperfusión, contrario al FNT-α, que se incrementa hasta el día 7, mientras que la ICAM-1 aumentó en todas las fases. CONCLUSIONES: En este estudio piloto, el PIR disminuyó el daño por lesión por isquemia- reperfusión, aunque el mayor efecto se observó después de 72 horas. BACKGROUND: Remote ischemic preconditioning (RIP) in liver transplantation has been suggested experimentally as a strategy to reduce ischemia-reperfusion injury. OBJECTIVE: Evaluate the effect of RIP on liver graft in cadaveric donors and the impact of various inflammatory mediators in this process. METHOD: Ten liver transplantation recipients, 5 controls and 5 PIR, were made in the cadaver donors by applying a pneumatic tourniquet in the upper third of both thighs for a period of 10 minutes followed by 10 minutes reperfusion. The determination of interleukine (IL)-1, IL-6, tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), intracellular adhesion molecule (ICAM)-1 was performed as well as hematological and biochemical parameters at various stages of liver transplantation. RESULTS: Significant increase of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase in the early stages of post-liver transplantation were observed, after 72 hours subjects who received liver transplantation subjected to RIP they showed a better response, which was also evident in platelet recovery, which persisted until phase 3 months in this group. IL-6 appears to participate in the early stages of the ischemia-reperfusion injury, contrary to TNF-α that increases until day 7 while ICAM-1 was increased in all phases. CONCLUSIONS: In this pilot study the PIR decreased the damage by ischemia-reperfusion injury, although the greatest effect was observed after 72 hours.

Is Ischemic Preconditioning a Useful Therapeutic Strategy in Liver Transplantation? Results from the First Pilot Study in Mexico.

BACKGROUND AND AIMS: The protective effect of ischemic preconditioning (IP) in liver transplantation (LT) has been studied with controversial results. We undertook this study to investigate whether IP of cadaveric donor livers is protective to allografts. METHODS: IP (LT + IP, n = 6) was induced by 10-min hilar clamping. These were compared to cadaver donors with no IP (LT, n = 7). Clinical data and blood were obtained in donors and recipients for biochemical and inflammatory mediator (IM) measurements (P-selectin, leukotriene B4, myeloperoxidase, ICAM-1, IL-1, IL-6, and TNF-α). Liver tissue samples were obtained from donors and recipients (90 min after reperfusion). RESULTS: No significant differences were found in demographic characteristics between donors and recipients. When comparing both groups (LT + IP vs. LT only), ICU stay was longer in LT + IP group. For biochemical parameters, a significant difference was found only with a higher total bilirubin at postoperative day 3 in LT + IP group. There was no statistical difference in IM between LT and LT + IP groups at different stages of the study. Histological analysis of donor grafts indicated the presence of steatosis (50%) in one graft from the LT + IP group. However, in post-reperfusion biopsies neither neutrophil infiltration nor grade of necrosis showed significant difference between groups. No incidence of primary graft nonfunction (PGNF) was observed and graft and patient survival was similar in the two groups at 24 months. CONCLUSION: IP does not seem to protect against I/R injury in cadaveric LT, and no PGNF was seen.