I TUOI DATI
I TUOI ORDINI
N. prodotti: 0
Totale ordine: € 0,00
I TUOI ABBONAMENTI
I TUOI ARTICOLI
Rivista di Angiologia
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
International Angiology 2000 June;19(2):166-70
Pathological changes of hepatic artery and portal vein, after allyl-alcohol and carbon tetrachloride administration. An experimental study
Papalambros E., Felekouras E., Tsamandas A. *, Sigala F., Salakou S. *, Tepetes K. *, Filis K., Milonakis M., Kourelis T. *, Bastounis E.
From the First Department of Surgery and Department of Histology, University of Athens Medical School Laiko General Hospital,
* Department of Pathology, University of Patras Medical School, Greece
Full text temporaneamente non disponibile on-line. Contattaci
Background. Alllyl-alchool (AA) and carbon tetrachloride (CC14) are known to cause peritoneal and pericentral liver necrosis, respectively. This study investigates pathological changes of hepatic artery and portal vein after simultaneous administration of AA and CC14 in rats.
Methods. The study comprised 130 male Wistar rats divided randomly into 2 groups: I (n=10) sham and II (n=120) AA injection (intraperitoneally: 0.62 mmol/kg) and rhinogastric administration of CC14 (0.66 ml/kg, 1:1 volume dilution in corn oil). After injection was completed, animals of group II were assigned in 12 categories and sacrificed 2, 4, 6, 12, 18, 24, 33, 48, 57, 81, and 153 hrs after. Tissue was obtained from the left anterior lobe and the hilum of the liver, and histological examination included H&E, silver methenamine and van Giesson stains.
Results. Liver sections from group II (AA+CC14) demonstrated periportal together with pericentral necrosis; the peak was 57 hrs after injection. In all 120 cases, H&E stain showed evidence of regeneration originated from zone 2, extending to zone 1 and occasionally to zone 3, and accomplished mainly by non-necrotic cell proliferation. Sections from the liver hilum showed thrombosis of the portal vein, whereas the hepatic artery and its branches developed a variety of changes. Initially (2, 4 hrs), endothelial hypertrophy was observed which was followed by focal fibrinoid necrosis of the arterial wall (6 hrs). Later on (9-153 hrs) the following findings were present: hyperplasia and non-isometric cytoplasmic vacuolisation of media, disruption of the elastic lamina, aggregation of foam cells and macrophages in intima, media, and focally in adventitia of hepatic artery; and lymphocytic inflammation of intimal and periadventitial area. In 2 cases (153 hrs) hepatic artery thrombosis was present.
Conclusions. Additionally to liver parenchymal changes, simultaneous administration of allyl-alcohol and carbon tetrachloride in rats results to vascular changes mainly in the hepatic artery and its branches. During liver parenchymal regeneration, the hepatic artery and its branches develop microscopic features that morphologically resemble those of atherosclerosis. These changes may result in hepatic artery thrombosis and or obstruction.