To elucidate early changes and the mechanism of ischaemia-reperfusion liver injury, we investigated three-dimensional microstructural changes of cellular actin filaments in rat livers using confocal laser scanning microscopy. The liver tissues of a reperfusion group were examined 12 h after removal of a vascular clamp. Fixed tissues were stained with fluorescein-labelled phalloidin to obtain stereoscopic images of the actin filaments and these were compared with histological findings. The images of bile canaliculi showed that multiple abnormal minute diverticula arose from the canalicular membranes and fused with one another, resulting in irregular dilation of the bile canaliculi. These changes were observed after 15 min of ischaemia and reperfusion in which no significant necrosis was seen. The frequency and degree of these changes were strictly dependent on the periods of ischaemia (15-60 min). We called these bile canacilular lesions "varicoid changes". The liver of an ischaemia group taken after persistent clamping without reperfusion did not show these changes. Our findings suggest that the varicoid change in the bile canaliculi is probably due to alterations in the actin polymerization-depolymerization cycle and is a pathognomonic change of ischaemia-reperfusion liver injury.
Living-related renal transplantation is the optimal therapy for patients with end-stage renal disease (ESRD). Normally, complications are rare in living-related donor nephrectomy. However, we experienced a case of pulmonary embolism (PE). The incidence of PE in living donor nephrectomy is rare, but the total incidence of PE in surgical operations has recently increased. The patient in the case reported here was diagnosed relatively early and recovered with appropriate treatment. It is very important for surgeons to realize that serious complications such as PE can develop in any case of living donor nephrectomy.
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