Histological and biochemical alterations in early-stage lobar ischemia-reperfusion in rat liver

Abstract

AIM:To investigate the structural and biochemical changes in the early stage of reperfusion in the rat livers exposed to lobar ischemia-reperfusion (IR). METHODS:The median and left lobes of the liver were subjected to 60 min ischemia followed by 5, 10, 30, 45, 60 and 120 min reperfusion. Blood samples were taken at different time intervals to test enzyme activities and biochemical alterations induced by reperfusion. At the end of each reperfusion period, the animals were killed by euthanasia and tissue samples were taken for histological examination and immunohistochemistry. RESULTS:Cell vacuolation, bleb formation and focal hepatitis were the most important changes occur during ischemia. While some changes including bleb formation were removed during reperfusion, other alterations including portal hepatitis, inflammation and the induction of apoptosis were seen during this stage. The occurrence of apoptosis, as demonstrated b y a p o p t o t i c c e l l s a n d b o d i e s , w a s t h e m o s t important histological change during reperfusion. The severity of apoptosis was dependent on the time of reperfusion, and by increasing the time of reperfusion, the numbers of apoptotic bodies was significantly enhanced. The amounts of lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, creatinine and urea were significantly increased in serum obtained from animals exposed to hepatic IR. CONCLUSION:In f l a m m a t i o n a n d s u b s e q u e n t apoptotic cell death were the most important changes in early-stage hepatic reperfusion injury, and the number of apoptotic bodies increased with time of reperfusion.

Protective effects ofHammada scopariaflavonoid-enriched fraction on liver injury induced by warm ischemia/reperfusion

“…These two processes lead to the generation of oxygen free radicals (Arab et al, 2009;Nishikawa et al, 2009;Ozmen et al, 2009). Postconditioning provides the liver with several cycles of on/off flow before reperfusion to control the generation of oxygen free radicals.…”

Attenuation of Reperfusion-Induced Hepatocyte Apoptosis is Associated with Reversed bcl-2/bax Ratio in Hemi-Hepatic Artery-Preserved Portal Occlusion

“…However, such maneuver is often insufficient in cases of excessive reperfusion injury following warm ischemia, and the reperfusion-induced hepatocyte apoptosis plays a paramount role in postoperative liver dysfunction [6]. Multiple modalities have been available to alleviate additional reperfusion injuries, primarily including ischemic preconditioning and the use of preservation fluid and cytoprotective agents [7][8][9][10].…”

“…The ischemia-reperfusion injury results from cellular necrosis as well as, and more importantly, apoptosis, a noninflammatory programmed cell death regulated by intrinsic genes [6]. The biochemical processes and genetic pathways remain relatively constant in the process of apoptosis although the molecular signaling mechanism involved is quite variable, including the upregulation or downregulation of bcl-2, bax, Fas, FasL, and p53 [12].…”

Ischemic Preconditioning Attenuates Morphological and Biochemical Changes in Hepatic Ischemia/Reperfusion in Rats

“…In the present study, the occurrence of apoptotic cells is associated with inflammatory reactions and reactive oxygen species (ROS) stress, which result in the activation of the apoptotic pathway mediated by mitochondria. Most recently, Arab et al [36] demonstrated that hepatic parenchyma is able to resist against some types of I/R injury and parenchymal cells are not susceptible to I/R injury, indicating the cell death by apoptosis is the most important change in the early phase after hepatic reperfusion injury. In the present study, a number of apoptotic cells did not increase remarkably after reperfusion in the CC group, partly because 60 min of 70% hepatic warm ischemia is insufficient to induce heavy liver injury.…”