Hepatic microcirculation during transient hepatic venous occlusion--intravital microscopic observation using hepatic vein clamp model in the mouse.

The purpose of this experiment was to evaluate the etiology of hepatic dysfunction in patients difficult to wean from cardiopulmonary bypass. We hypothesized that increased central venous pressure and subsequent hepatic congestion during weaning from cardiopulmonary bypass would lead to hepatic dysfunction. To induce hepatic congestion in mice, we clamped the hepatic vein for fifteen min, and observed the microcirculation of the liver using an intravital microscope during clamping and the following 30 min of reperfusion. During reperfusion, non-reflow phenomenon, leukocytes adhesion to the wall of sinusoids, erythrocytes sludging, acute swelling of hepatic cells and narrowing of sinusoids were observed. These phenomena were indicative of warm ischemia-reperfusion injury of the liver itself. Based on these findings we concluded that, after repeated episodes of warm ischemia and reperfusion of the liver, hepatic cells would be damaged, and finally hepatic dysfunction was induced. To prevent hepatic dysfunction, repeated attempts to wean the patient from cardiopulmonary bypass should be avoided and increases central venous pressure should be prevented by early use of cardiopulmonary support.