The central role of sinusoidal endothelial cells in hepatic hypoxia-reoxygenation injury in the rat

Abstract

Reperfusion injury is the phenomenon whereby relief of The role of individual cell types in hepatic hypoxiahypoxic ischemia is followed by accentuation rather than rereoxygenation (reperfusion) injury has not been comlief of tissue damage. This paradoxical event is well docupletely defined. We therefore examined the effects of mented in the intact liver and has considerable clinical relehypoxia and hypoxia-reoxygenation on the viability of vance in relation to organ preservation and hepatic surgery. SECs in producing liver cell injury during hypoxia-reoxygen- Received November 8, 1995; accepted July 1, 1996. ation were studied by coculture experiments.Dev

Effect of cold hypoxic storage and reoxygenation at 37°C of cultured precision-cut rat liver slices on paracetamol metabolism

“…Nevertheless, our results show that Kuper cells were neither activated by cold preservation nor by changes in oxygen tension and temperature. Such ®ndings are in agreement with Samarasinghe and Farrell (1996), who reported that in vitro hypoxia-reoxygenation does not activate Kuper cells to secrete superoxide radicals or other cytotoxic products. Since protein synthesis is very sensitive to changes in oxygen tension (Lefebvre et al 1993), and because the level of ATP during cold storage is low, it is not surprisingly that protein synthesis rates were rather decreased after cold preservation.…”

Toxicity of low dose azathioprine and 6-mercaptopurine in rat hepatocytes. Roles of xanthine oxidase and mitochondrial injury

“…Rats were housed under constant temperature (22 8C) and humidity with a 12-h light/dark cycle, fed commercial rat pellets (Allied Foods, Sydney, Australia) and allowed food and water ad libitum. Liver cells were isolated by nonrecirculating collagenase perfusion of rat liver through the portal vein [17], as reported [10,16,18]. Viability (by trypan blue exclusion) always exceeded 80%.…”

FGL2/Fibroleukin mediates hepatic reperfusion injury by induction of sinusoidal endothelial cell and hepatocyte apoptosis in mice

“…FcγRIIB -/-WT longed re-oxygenation [35][36][37]. Samarasinghe et al [36] compared in vitro the susceptibility of different liver cell types to hypoxia and found that SEC were even more resistant to prolonged hypoxic injury than hepatocytes or Kupffer cell.…”

“…Samarasinghe et al [36] compared in vitro the susceptibility of different liver cell types to hypoxia and found that SEC were even more resistant to prolonged hypoxic injury than hepatocytes or Kupffer cell. In their study only 10% of SEC underwent cell death despite 24 h hypoxia (PO 2 <1 mm Hg), and even after 8 h hypoxia and 24 h of re-oxygenation only 40% of the SEC expressed features of necrotic cell death.…”