title: [Changes in the intraorganic vessels of the liver in acute experimental peritonitis].
abstract: Structural pathology and hemodynamics in the livers of 110 white rats were studied histologically, electron microscopically and histoautoradiographically during 5 days since the onset of acute experimental peritonitis. This was accompanied with distinct structural and functional derangement of histohematic barrier along with hepatic hemodynamic disturbances dependent in severity on both fecal suspension quantity and AEP course and stage. Pathologic and compensatory-adaptive reactions profile was established for the animals intrahepatic circulation. Polymorphism of the vascular affections underlies the emergence of the two morphogenetic mechanisms responsible for impairment of hepatic parenchyma: 1) a direct action of toxic substances on hepatocytic cellular membranes, 2) disordered circulatory-hypoxic effect based on pronounced DIC-syndrome and thrombosis. The former mechanism gives rise to disseminated necrosis of hepatocytes, while the latter entails the onset of intralobular necrotic foci, typical for the reactive and toxic stages of acute peritonitis, respectively.
authors.forename: G S
authors.initials: GS
authors.lastname: Ivanova
authors.forename: V I
authors.initials: VI
authors.lastname: Glumov
authors.forename: A K
authors.initials: AK
authors.lastname: Kranchev
authors.forename: V L
authors.initials: VL
authors.lastname: Bazhenov
mesh_terms: D000208:Acute Disease; D000818:Animals; D001158:Arteries / Q000648:ultrastructure; D001345:Autoradiography; D004211:Disseminated Intravascular Coagulation / Q000209:etiology / Q000473:pathology; D005260:Female; D008099:Liver / Q000098:blood supply* / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D009336:Necrosis; D010538:Peritonitis / Q000150:complications / Q000473:pathology*; D051381:Rats; D013997:Time Factors; D014680:Veins / Q000648:ultrastructure
vernacular_title: Izmeneniia vnutriorgannykh sosudov pecheni pri ostrom éksperimental'nom peritonite.