Ultrastructural changes in rat liver sinusoids during prolonged normothermic and hypothermic ischemia in vitro.

By means of electron microscopic analysis of liver fragments incubated in an air-tight wrapping (in vitro ischemia), the following facts have been established with regard to the development of signs of irreversible damage in cells from the sinusoidal wall compared with hepatocytes. With normothermic (37 degrees C) in vitro ischemia, signs of irreversible damage appeared in cells of the sinusoidal wall at a a much earlier stage than in hepatocytes (60-90 min and 90 min-2 h respectively). With in vitro ischemia in the cold (4 degrees C), these differences were even more marked; irreversible cell damage was apparent after between 24 and 36 h incubation in endothelial cells, whereas in hepatocytes flocculent densities followed by other signs of irreversible damage were found only after 79 h incubation. These findings are discussed in relation to the 'no reflow' phenomenon after ischemia in general. The rule that changes in the vascular system following ischemia may well obscure the actual sensitivity of parenchymal cells is particularly applicable to the liver. Attempts to lengthen the period of ischemia which 'liver tissue' can stand for example, with a view to transplantation, attention should be focussed primarily on the events in the sinusoidal wall.