Hepatic Microcirculation in Inflow and Inflow–Outflow Occlusion of the Liver

• Published in: Transplantation proceedings 2013-03, Vol.45 (2), p.474-479
• Main Authors: Koc, E, Topaloglu, S, Calik, A, Sokmensuer, C, Abdullazade, S, Karabulut, E, Piskin, B
• Format: Article
• Language: English
• Subjects: Alanine Transaminase - blood; Animals; Aspartate Aminotransferases - blood; Biomarkers - blood; Blood Flow Velocity; L-Lactate Dehydrogenase - blood; Laser-Doppler Flowmetry; Liver - blood supply; Liver - enzymology; Liver - pathology; Liver - surgery; Liver Circulation; Liver Transplantation - adverse effects; Male; Microcirculation; Rats; Rats, Wistar; Reperfusion Injury - blood; Reperfusion Injury - etiology; Reperfusion Injury - pathology; Reperfusion Injury - physiopathology; Surgery
• ISSN: 0041-1345; 1873-2623
• DOI: 10.1016/j.transproceed.2012.07.155

Abstract Background Total vascular exclusion (TVE) causes warm liver ischemia. The aim of this study was to investigate the patterns of injury caused by inflow-outflow obstruction in the rat liver. Materials and Methods Twenty-four Wistar-Albino rats were divided into three groups: liver inflow occlusion (Group A), inflow-outflow occlusion (Group B) and intermittent inflow-outflow occlusion applied for 15 minutes. Microcirculation was measured with laser Doppler flowmetry during the procedure. Samples for biochemical and histopathological analyses were collected at the end of the ischemia period. Results Significant alterations in microcirculation were determined by application of vascular control maneuvers. Microcirculation in the central and dome segments were affected adversely compared with the dome segments in all experimental groups. TVE induced severe disturbances in hepatic microcirculation with more prominent hepatocellular damage. Damage to central segments of the rat liver was more prominent with inflow occlusion; whereas inflow-outflow occlusion produced more prominent damage to dome segments. Intermittent application of TVE clamping was associated with more hepatocellular damage compared with continuous TVE. Conclusion Our mapping methodology within the liver parenchyma suggested that hepatovenous back-perfusion is a principle source of continuity of microcirculation in the rat liver during inflow occlusion. Inflow-outflow occlusion caused more tissue damage compared with inflow occlusion. Ischemic preconditioning during TVE did not increase the tolerance of the liver against ischemia.