Changes in hepatic lymph vessels in endotoxaemia.
This study was undertaken into rats to investigate changes in the hepatic lymph vessels and the space of Disse in endotoxaemia and to examine their relationship with the development of endotoxin-induced hepatic injury. Lymph stasis, namely dilatation of the lymph vessels and oedema, developed rapidly in the medium-sized portal canals, the large portal canals, and the liver hilum after endotoxin injection, but not in the small portal canals. Such changes reached their maximum 4-8 h after endotoxin injection and had recovered markedly by 16 h after the injection. The space of Disse remained within normal limits during this period. These findings suggest that the intrahepatic lymph stasis in endotoxaemia may be caused by a reduction in the pumping activity of the extrahepatic and the intrahepatic large lymph vessels rather than by an increase of lymph formation in the liver lobules. There was no evidence suggesting a direct relationship between the disturbance of hepatic lymph flow and the development of hepatic injury in endotoxaemia.
Shibayama
Y
Y
Department of Pathology, Osaka Medical College, Japan.
Urano
T
T
Nakata
K
K
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood*; D008099:Liver / Q000473:pathology*; D008208:Lymphatic System / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D012709:Serum Albumin / Q000378:metabolism; D012772:Shock, Septic / Q000097:blood / Q000378:metabolism / Q000473:pathology*
D001798:Blood Proteins; D004731:Endotoxins; D012709:Serum Albumin; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase