Postconditioning in Liver Ischemia-Reperfusion Injury
Roberto Teixeira*, Nilza Molan, Marcia S. Kubrusly, Marta Privato, Ana Maria M. Coelho, Telesforo Bacchella, Marcel C. Machado
University of Sao Paulo, Sao Paulo, Brazil
Introduction: Liver ischemia-reperfusion injury (LIRI) is a process present in several events like liver resections, transplantation, shock and sepsis. Ischemia-reperfusion injury is a complex cascade of interactions that results in alteration of many different organs. The restoration of blood flow may lead to local and sistemic injury. Several techniques have been developed in order to avoid or ameliorate LIRI in clinical situations. Preconditioning, intermittent vascular occlusion, anti TNF-alpha and antioxidants have been tested with limited clinical results. Postconditioning is the application of a gradual, staged or stutter reperfusion after the ischemic lesion. Postconditioning alters the hydrodynamics of early reperfusion and stimulates endogenous mechanisms that attenuate the reperfusion injury. OBJECTIVE: To evaluate the local and systemic potential protective effect of postconditioning in liver ischemia-reperfusion injury in rats.
Methods: Hepatic anterior pedicle of median and left anterolateral segments were exposed and clamped with an atraumatic vascular bulldog clamp for one hour. Two hours later, clamp was released in two different ways: Control Group (n=7): clamp was release straightforward; Postconditioning Group (n=6): clamp was released intermittently, in 5 periods of 5 seconds open, followed of 5 seconds of closure. Hepatic liver enzymes, serum TNF-α and interleukins, pulmonary myeloperoxidase, malondialdehyde (MDA) and GST-α3 gene expression were studied.
Results: There was no significant difference for all analysis between control and postconditioning groups except for MDA analysis. Lipidic peroxidation was reduced in the ischemic and non-ischemic liver by postconditioning.
Conclusion: Postconditioning reduces LIRI in the ischemic and non-ischemic liver in this model. This protective action is independent of cytokines and TNF production. Further studies will be addressed to clarify this issue.