title: [Changes in the Kupffer cells after reversible ischemia of the liver in rats].
abstract: Portal vein occlusion leads to accumulation of intestinal endotoxin in the portal vein that may be a trigger for release of liver macrophage products from the cells and then for damage to hepaparenchyma. There is activation of Kupffer cells (KC) after ischemia, increasing the volume of second lysosomes, severe erythrophagia was also seen. Moreover, there is an increase in KC count and appearance of young liver macrophages. The rise of KC population counts due to the increased number of functional element play a positive role in clearance of intestinal endotoxin and liver defence for ischemic and recirculatory organ damage.
authors.forename: I A
authors.initials: IA
authors.lastname: Sokirchenko
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D004912:Erythrocytes / Q000648:ultrastructure; D007511:Ischemia / Q000473:pathology*; D007728:Kupffer Cells / Q000648:ultrastructure*; D008099:Liver / Q000098:blood supply*; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology; D013997:Time Factors
vernacular_title: Izmeneniia kletok Kupfera posle obratimoĭ ishemii pecheni krys.