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Adenosine Triphosphate in Experimental Liver Surgery (pp. 123-142) $0.00
Authors:  (M. Elias-Miró, M.B. Jiménez-Castro, C. Peralta, Institut d´Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain, and others)
The shortage of organs has led centers to the acceptance of marginal grafts such as
fatty livers, small-for-size liver or aged donors. However, the clinical problem is
unresolved since this type of liver tolerates poorly hepatic ischemia-reperfusion (I/R) and
show regenerative failure after liver surgery. The use of marginal liver for transplant is
associated with increased risk of primarily non-function or dysfunction after surgery,
being the deficiencies in energy metabolism one of the main mechanisms responsible for
the vulnerability of this liver type to I/R injury and regenerative failure. Indeed,
experimental studies and clinical observations clearly indicate that marginal livers show
more adenosine triphosphate (ATP) depletion during ischemia and synthesize
less ATP than normal livers during the early phase of reperfusion. This book chapter will
be focused on the role of ATP in hepatic I/R injury and the mechanisms responsible
of ATP depletion in both marginal and normal livers. We will show that the deleterious
effects of ischemia on ATP depletion and the lactate production limit survival of
hepatocytes, being this effect more exacerbated in marginal livers. Also, we will explain
how different conditions, including the presence of fatty infiltration or starvation,
affect ATP recovery during reperfusion, a prerequisite for liver graft viability after
surgery. In hepatic I/R injury cell death can occur via necrosis or apoptosis. We will
review the key role of ATP as a putative apoptosis/necrosis switch: when ATP depletion
is severe, necrosis ensues before the activation of the energy-requiring apoptotic
pathway. The present book chapter will discuss how ATP depletion and its posterior
restoration depends on the type of ischemia (cold or warm ischemia), the type of liver,
duration and the extent of hepatic ischemia, starvation, and the presence of liver
regeneration. We will show that the mechanism responsible for ATP recovery during
reperfusion depends of the experimental model used. Therefore, is very important to
choose to standardize experimental conditions according to the clinical question being
answered. As the decrease in ATP immediately after partial hepatectomy associated with
reduced-size liver transplantation trigger a signal to activate the catabolism of existing
peripheral adipose stores; we will review how lipid accumulation is used
for ATP synthesis, necessary for liver regeneration. Finally, we will consider
pharmacological and surgical strategies that prevent ATP degradation and/or
increase ATP restoration during reperfusion as this may improve the post-transplant
outcomes and could reduce waiting list for liver transplantation. 

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Adenosine Triphosphate in Experimental Liver Surgery (pp. 123-142)