Volume 38, Issue 1, Pages 59-66 (January 2003) Ischemic preconditioning protects from hepatic ischemia/reperfusion-injury by preservation of microcirculation and mitochondrial redox-state  Matthias Glanemann, Brigitte Vollmar, Andreas K Nussler, Thilo Schaefer, Peter Neuhaus, Michael D Menger  Journal of Hepatology  Volume 38, Issue 1, Pages 59-66 (January 2003) DOI: 10.1016/S0168-8278(02)00327-6

Fig. 1 Kinetics of latex particle clearance by intrahepatic Kupffer cells in animals subjected to 45 min of global hepatic ischemia and 90 min of reperfusion, as assessed by intravital microscopy after intra-arterial injection of fluorescently labeled latex particles. Filled squares represent IP-animals (n=7), which were treated by ischemic preconditioning (5 min global hepatic ischemia followed by 30 min of reperfusion) before induction of the sustained period of 45 min of ischemia. Open squares indicate sham controls, which were time-matched, but not treated by IP (n=7). Means±SEM; #P<0.05 vs. sham-treated animals (open squares). Journal of Hepatology 2003 38, 59-66DOI: (10.1016/S0168-8278(02)00327-6)

Fig. 2 (A) Venular leukocyte rolling (%) and (B) venular leukocyte adherence (n/mm2) in animals subjected to 45 min of global hepatic ischemia and 90 min of reperfusion, as assessed by intravital fluorescence microscopy after in vivo leukocyte staining with rhodamine 6G. Filled bars represent IP-animals (n=7), which were treated by ischemic preconditioning (5 min global hepatic ischemia followed by 30 min of reperfusion) before induction of the sustained period of 45 min of ischemia. Open bars indicate sham animals, which were time-matched, but not treated by IP (n=7). Means±SEM; *P<0.05 vs. basal. Journal of Hepatology 2003 38, 59-66DOI: (10.1016/S0168-8278(02)00327-6)

Fig. 3 (A) Sinusoidal perfusion (%) and (B) hepatocellular NADH fluorescence (aU) in animals subjected to 45 min of global hepatic ischemia and 90 min of reperfusion, as assessed by intravital multifluorescence microscopy. Filled bars represent IP-animals (n=7), which were treated by ischemic preconditioning (5 min global hepatic ischemia followed by 30 min of reperfusion) before induction of the sustained period of 45 min of global ischemia. Open bars indicate sham animals, which were time-matched, but not treated by IP (n=7). Means±SEM; *P<0.05 vs. basal; #P<0.05 vs. sham-treated controls (open bars). Journal of Hepatology 2003 38, 59-66DOI: (10.1016/S0168-8278(02)00327-6)

Fig. 4 Regression analysis between sinusoidal perfusion (%) and hepatocellular NADH fluorescence (aU) in animals subjected to 45 min of global hepatic ischemia and 90 min of reperfusion. Analysis includes data assessed at baseline (before ischemia) and at 30 min and 90 min of reperfusion. Filled squares represent IP-animals (n=7), which were treated by ischemic preconditioning (5 min global hepatic ischemia followed by 30 min of reperfusion) before induction of the sustained period of 45 min of global ischemia. Open squares indicate sham animals, which were time-matched, but not treated by IP (n=7); r=regression coefficient; r=−0.75 (P<0.001) for all data analyzed; subgroup analysis revealed r=−0.78 (P<0.001) and r=−0.62 (P<0.005) for sham and IP-animals, respectively. Journal of Hepatology 2003 38, 59-66DOI: (10.1016/S0168-8278(02)00327-6)