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. 2014 Aug;3(4):179-84.
doi: 10.3978/j.issn.2304-3881.2014.06.03.

Role of ischemic preconditioning in hepatic ischemia-reperfusion injury

Affiliations

Role of ischemic preconditioning in hepatic ischemia-reperfusion injury

Valeriy V Boyko et al. Hepatobiliary Surg Nutr. 2014 Aug.

Abstract

Background: Investigation into less traumatic method of vascular occlusion during liver resection is the actual problem in hepatic surgery because of high level of complications such as liver failure. In this connection, the goal of our study was to determine the optimal model of vascular clamping. The research showed that vascular occlusion with ischemic preconditioning in the mode 5/10/15 the most delicate technique.

Methods: Forty white giant rabbits were divided randomly into four groups (n=10 in each group). In group I we used continuous Pringle maneuver by 30 min. In group II we used intermittent Pringle maneuver: 15 min of clamping/5 min of unclamping (reperfusion)/15 min of clamping. In group III we used intermittent Pringle maneuver with ischemic precondition: 5 min of ischemia/5 min of reperfusion, 10 min of ischemia/5 min of reperfusion/15 min of ischemia. Group IV (control group) is without hepatic ischemia. All animals were performed a liver biopsy at the end of the surgery. Five rabbits from each group underwent re-laparotomy on day 3 after surgery with biopsy samples being taken for studying reparative processes in liver parenchyma.

Results: Results of morphometric analysis were the best to illustrate different level of liver injury in the groups. Thus, there were 95.5% damaged hepatocytes after vascular occlusion in hepatic preparations in group I, 70.3% damaged hepatocytes in group II, and 42.3% damaged hepatocytes in group III. There were 5.3% damaged hepatocytes in the control group.

Conclusions: Vascular occlusion with ischemic preconditioning in the mode 5/10/15 the most delicate technique that does not involve major structural injuries and functional disorders in the remnant liver. Thus, it is amenable to translation into clinical practice and may improve outcomes in liver resection with inflow vascular occlusion.

Keywords: Liver resection; Pringle maneuver; ischemia-reperfusion injury; ischemic preconditioning; vascular occlusion.

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Figures

Figure 1
Figure 1
Ischemia/reperfusion time of the groups.
Figure 2
Figure 2
Design of the experimental model.
Figure 3
Figure 3
Hepatocyte cytoplasm contains glycogen. Nuclei with pronounced karyolemma and clumpy karyoplasm structure. Diploid cells are present. Group IV (reference). Staining with haematoxylin and eosin (×200).
Figure 4
Figure 4
Trabecular decomplexation and diffuse necrobiotic and necrotic hepatocyte changes. Group I. Staining with haematoxylin and eosin (×200).
Figure 5
Figure 5
Zones of cells with pronounced alterative changes alternating zones with low number of injured cells. Staining with haematoxylin and eosin. Group II (×200).
Figure 6
Figure 6
Central zone of the lobule with great number of unchanged cells, peripheric zone with signs of trabecular decomplexation and hepatocytes with alterative changes. Staining with haematoxylin and eosin. Group III (×200).
Figure 7
Figure 7
Hepatocyte cytoplasm contains glycogen in the form of clumpy crimson red deposits. Group IV (reference). Periodic acid Schiff reaction (×200).
Figure 8
Figure 8
Glycogen in hepatocyte cytoplasm is not detected or is traced. Group I. Staining with haematoxylin and eosin (×200).
Figure 9
Figure 9
Complete absence of hepatocyte nuclei staining. Group I. Staining by the Feulgen-Rossenbeck reaction for DNA (×400).
Figure 10
Figure 10
Moderate staining of hepatocyte nuclei. Nuclei of Kupffer’s cells are intensively stained. Group III. Staining by the Feulgen-Rossenbeck reaction for DNA (×400).
Figure 11
Figure 11
Number of damaged hepatocytes in sight of the 30 cells in hepatic preparations. Biopsy after clamping.
Figure 12
Figure 12
Number of damaged hepatocytes in sight of the 30 cells in hepatic preparations. Biopsy on day 3 after clamping.

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