Preoperative assessment of liver function: a comparison of 99mTc-Mebrofenin scintigraphy with indocyanine green clearance test.

BACKGROUND/AIMS: The indocyanine green (ICG) clearance test is the most frequently used test for preoperative assessment of liver parenchymal function but has its limitations. The aim of this study was to investigate the correlation between ICG clearance test and the liver uptake of 99-Technetium-labelled (99mTc)-Mebrofenin (99mTc-Mebrofenin) as measured with hepatobiliary scintigraphy. METHODS: Fifty-four patients were diagnosed as hepatocellular carcinoma (n=9), hilar tumours (n=20) and 25 patients with non-parenchymal tumours including colorectal metastasis (n=15) and miscellaneous tumours (n=10). One day prior to operation, hepatobiliary 99mTc-Mebrofenin scintigraphy was performed after intravenous injection of 85 MBq and the 15-min clearance rate of ICG (ICG-C15) was measured. RESULTS: The mean ICG-C15 was 86.86+/-1.19% (SEM). The mean 99mTc-Mebrofenin uptake rate was 12.87+/-0.52%/min. A significant correlation was obtained between 99mTc-Mebrofenin uptake rate by scintigraphy and ICG-C15 (r=0.73, P<0.0001). The mean clearance capacity of the right liver segments (79.83+/-1.63, range 47.75-95.97%) was larger than that of the left segments (20.24+/-1.55, range 6.51-52.51%). CONCLUSION: 99mTc-Mebrofenin uptake rate as assessed by scintigraphy is an efficient method for determining liver function and correlates well with ICG clearance. At the same time, 99mTc-Mebrofenin scintigraphy provides information of segmental functional liver tissue, which is of additional use when planning liver resection.

Decrease in core liver temperature with 10 degrees C by in situ hypothermic perfusion under total hepatic vascular exclusion reduces liver ischemia and reperfusion injury during partial hepatectomy in pigs.

OBJECTIVE: We attempted to assess liver ischemia/reperfusion injury under a mild decrease in core liver temperature of 10 degrees C by in situ hypothermic perfusion during ischemia. METHODS: Liver ischemia was induced in pigs by total hepatic vascular exclusion with concomitant in situ perfusion with hypothermic (4 degrees C) Ringer-glucose (cold perfused group, core liver temperature maintained at 28 degrees C), with normothermic (38 degrees C) Ringer-glucose (warm perfused group) or without in situ perfusion (control group). RESULTS: In the cold perfused, warm perfused, and control groups, 24-hour survival was 5/5, 0/5, and 3/5, respectively. Hemodynamic parameters in the cold perfused group remained stable, whereas pigs in both other groups required circulatory support. Plasma AST and interleukin-6 levels were lower in the cold perfused group than in both other groups. Hepatocellular function was best preserved in the cold perfused group as indicated by complete recovery of bile production during reperfusion and no loss of indocyanine green clearance capacity. In both other groups, bile production and indocyanine green clearance capacity were reduced significantly. The hyaluronic acid uptake capacity of pigs in the cold perfused group or control group did not differ, indicating preserved sinusoidal endothelial cell function. Histopathologic injury scores during reperfusion were significantly lower in the cold perfused group when compared to both other groups. CONCLUSIONS: A mild decrease in core liver temperature of 10 degrees C by in situ hypothermic liver perfusion during ischemia protects the liver from ischemia/reperfusion injury. This protection appears to be related to cooling of the liver rather than to the washout of blood during perfusion.

Effect of in situ hypothermic perfusion on intrahepatic pO2 and reactive oxygen species formation after partial hepatectomy under total hepatic vascular exclusion in pigs.

AIM: This study examined attenuation of ischemia and reperfusion (I/R) induced liver injury during liver resections by hypothermic perfusion of the liver under total hepatic vascular exclusion (THVE). METHOD: Reactive oxygen species (ROS) formation, microcirculatory integrity and endothelial cell damage were investigated. Left hemihepatectomy (LHX) was performed without in situ perfusion (control-LHX, n = 5) or with concomitant in situ perfusion with hypothermic (4 degrees C) Ringer-glucose (cold-LHX, n = 5) or normothermic (38 degrees C) Ringer-glucose (warm-LHX, n = 5). Glutathione (GSH) and malondialdehyde (MDA) concentrations, tissue pO2 levels and hyaluronic acid (HA) uptake capacity were determined. RESULTS: After cold, warm and control-LHX, 24 h survival was 5/5, 0/5 and 3/5, respectively. GSH levels were best preserved after cold-LHX during reperfusion. MDA levels increased in all groups without significant differences between the groups during reperfusion. Tissue pO2 levels increased after cold-LHX whereas after warm-LHX and control-LHX, pO2 levels decreased during reperfusion. HA uptake capacity remained normal after cold-LHX. After warm-LHX and control-LHX, HA uptake capacity decreased after 6 h of reperfusion but recovered after 24 h of reperfusion in the control-LHX group. CONCLUSION: Moderate hypothermic perfusion protects the liver from I/R injury during LHX under THVE. This protective effect depended on maintenance of liver microcirculation rather than a reduction in ROS formation.

Influence of acidosis and hypoxia on liver ischemia and reperfusion injury in an in vivo rat model.

The contribution of acidosis to the development of reperfusion injury is controversial. In this study, we examined the effects of respiratory acidosis and hypoxia in a frequently used in vivo liver ischemia and reperfusion (I/R) injury rat model. Rats were anesthetized with intraperitoneal anesthetics and subjected to partial liver ischemia (70%) for 60 min and subsequent reperfusion for 90 min under the following conditions: 1) no acidosis and normoxia, maintained by controlled ventilation; 2) acidosis and normoxia, maintained by passive supply with oxygen; 3) no acidosis and hypoxia, maintained by bicarbonate administration without respiratory support; and 4) acidosis and hypoxia, i.e., without respiratory support or pH correction. Changes in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured as parameters of hepatocellular injury, and bile secretion was monitored. AST and ALT levels were lowest in the ventilated rats and highest in the bicarbonate-treated rats. No differences in bile secretion were found between groups. Our results suggest that respiratory acidosis significantly enhanced liver I/R injury under normoxic conditions, whereas respiratory acidosis significantly reduced liver I/R injury under hypoxic conditions.