The influence of organ temperature on hepatic ischemia-reperfusion injury

Background. Although hepatic ischemia-reperfusion (I/R) injury can be reduc ed by cooling of the ischemic organ, a systematic in vivo analysis of the i nfluence of organ temperature in I/R, injury is missing. The aim of this st udy was to systematically investigate the impact of defined temperatures of the ischemic liver tissue on microvascular I/R, injury. Methods. Ischemia of the left liver lobe was induced in C57BL/6 mice for 90 min. The ischemic lobe was placed in a polyethylene well and the temperatu re was adjusted to 37 degreesC, 26 degreesC, 15 degreesC, and 4 degreesC by superfusion with cooled/warmed saline solution. The ischemia groups (n=7 e ach) were compared with a sham-operated group (n=7). The sinusoidal perfusi on index and the number of leukocytes firmly adherent to the endothelium of postsinusoidal venules were assessed using intravital fluorescence microsc opy at 30 min, 120 min, and 240 min of reperfusion, respectively. At the en d of the experiment, serum activities of the liver enzymes aspartate aminot ransferase/alanine aminotransferase were determined, and tissue specimens w ere examined by electron microscopy. Results. Core body temperature did not differ significantly between the gro ups. In the 37 degreesC group, the sinusoidal perfusion index was significa ntly reduced and the number of adherent leukocytes was significantly increa sed compared with the sham group. In all hypothermia groups, however, the m icrocirculatory parameters did not differ from the sham group. Serum activi ties of aspartate aminotransferase/alanine aminotransferase were significan tly increased and hepatocellular integrity was severely affected in the 37 degreesC group as compared with all other groups. Conclusions. These findings demonstrate that in the mouse liver the known p rotective effect of hypothermia is already encountered at 26 degreesC. Furt her reduction of temperature did not generate additional protection from I/ R injury.