Volume 41, Issue 2, Pages (August 2004)

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Volume 41, Issue 2, Pages 299-306 (August 2004) The delay of rearterialization after initial portal reperfusion in living donor liver transplantation significantly determines the development of microvascular graft dysfunction  Gero Puhl, Klaus-D. Schaser, Daniel Pust, Katrin Köhler, Brigitte Vollmar, Michael D. Menger, Peter Neuhaus, Utz Settmacher  Journal of Hepatology  Volume 41, Issue 2, Pages 299-306 (August 2004) DOI: 10.1016/j.jhep.2004.04.017

Fig. 1 (A) In vivo visualization of the human hepatic microcirculation by OPS-imaging under physiological conditions. The contrast is obtained by the absorption of light by hemoglobin-containing cells, i.e. erythrocytes. Hence, the hemoglobin carrying cells appear in a negative contrast compared with the surrounding tissue, and imaging of parenchymal and endothelial cells, e.g. the vessel wall, is not possible. The erythrocytes are tightly packed as a column within the sinusoids, which represents the vascular lumen. The white arrows show the formation of a central venule branch by sinusoids and postsinusoidal venules. (B) After initial portal reperfusion the flow within the venules is bidirectional in dependence of the patients' respiration (bidirectional white arrows). The sinusoidal network is dramatically rarified when compared to the baseline perfusion. (C) Reperfusion of the hepatic artery results in rapid reopening of the sinusoids, which are mainly orthogradely perfused and appear dilatated compared to the baseline (black arrows). 30 min following rearterialization, residual stasis and erythrocyte sludging and extravasation by the mean of reperfusion injury could be observed (white arrows). Journal of Hepatology 2004 41, 299-306DOI: (10.1016/j.jhep.2004.04.017)

Fig. 2 Red blood cell velocity (RBCV) within human hepatic sinusoids under physiological conditions (BL), following initial portal reperfusion (PV) and at 5 min (HA5) and 30 min (HA30) after subsequent hepatic arterial reperfusion. Data are given in (μm/s) (A) and as percent change of baseline (B). + P<0.05 vs. baseline; # P<0.05 vs. initial portal reperfusion; o P<0.05 vs. 5 min hepatic arterial reperfusion. Journal of Hepatology 2004 41, 299-306DOI: (10.1016/j.jhep.2004.04.017)

Fig. 3 Sinusoidal diameters (D) within human hepatic sinusoids under physiological conditions (BL), following initial portal reperfusion (PV) and at 5 min (HA5) and 30 min (HA30) after subsequent hepatic arterial reperfusion. Data are given in (μm) (A) and as percent change of baseline (B). + P<0.05 vs. baseline; # P<0.05 vs. initial portal reperfusion. Journal of Hepatology 2004 41, 299-306DOI: (10.1016/j.jhep.2004.04.017)

Fig. 4 Sinusoidal volumetric blood flow (BVs) within human hepatic sinusoids under physiological conditions (BL), following initial portal reperfusion (PV) and at 5 min (HA5) and 30 min (HA30) after subsequent hepatic arterial reperfusion. Data are given in (pl/s) (A) and as percent change of baseline (B). + P<0.05 vs. baseline; # P<0.05 vs. initial portal reperfusion; o P<0.05 vs. 5 min hepatic arterial reperfusion. Journal of Hepatology 2004 41, 299-306DOI: (10.1016/j.jhep.2004.04.017)

Fig. 5 Functional sinusoidal density (FSD) within human hepatic sinusoids under physiological conditions (BL), following initial portal reperfusion (PV) and at 5 min (HA5) and 30 min (HA30) after subsequent hepatic arterial reperfusion. Data are given in (cm−1) (A) and as percent change of baseline (B). + P<0.05 vs. baseline; # P<0.05 vs. initial portal reperfusion. Journal of Hepatology 2004 41, 299-306DOI: (10.1016/j.jhep.2004.04.017)

Fig. 6 The Pearson product moment correlation between the PV–HA interval and the functional sinusoidal density (FSD) shows an inverse correlation (P<0.05,r=−0.66) (A). The longer the PV–HA interval, the more pronounced the decline of the FSD. In contrast, the perfused sinusoids were hyperemic with an increased volumetric blood flow, which positively correlated with the PV–HA interval (P<0.05,r=0.84) (B). The quality of the initial portal reperfusion significantly influences postoperative transaminase release. The worse the initial portal reperfusion, the higher the transaminase levels on postoperative day 2 (P<0.05,r=−0.62) (C) and day 3 (P<0.05,r=−0.72). Journal of Hepatology 2004 41, 299-306DOI: (10.1016/j.jhep.2004.04.017)