Liver injury by experimental portal bacteremia: histogenetic recovery study in the rat

To study the histogenetic recovery of hepatic lesions due to portal bacteremia, a complication of some clinical conditions, an experimental animal model had developed. Portal bacteremia was performed in 8-week rats and the morphological recovery of liver was histologically checked 1 to 6 days after bacteria inoculation. The major injuries, such as acute inflammatory exudate of the portobiliary spaces, piecemeal necrosis of muralium, micro-abscesses and areas of hepatocyte necrosis of the liver parenchyma, and thrombosis in the centrolobular vein were recorded 1 day after inoculation. Minimal signs of vacuolar degeneration, steatosis, necrosis areas, vessel congestion and focal hemosiderosis together with a small hepatocyte proliferative activity was instead appreciable with longer time. The results seem to suggest a role of vascular structures and Kupffer cells in the morphological repair. This experimental model could serve to understand better similar clinical hepatology conditions, such as portal bacteremia.

[1]  A. Aktekin,et al.  Liver Injury in Sepsis and Abdominal Compartment Syndrome in Rats , 2006, Surgery Today.

[2]  K. Hirata,et al.  Sepsis and cholestasis: basic findings in the sinusoid and bile canaliculus. , 2001, Journal of hepato-biliary-pancreatic surgery.

[3]  P. Watkins,et al.  Experimental models of Gram‐negative sepsis , 2001, The British journal of surgery.

[4]  G. Feuerstein,et al.  An improved clinically relevant sepsis model in the conscious rat , 2000, Critical care medicine.

[5]  W. Stremmel,et al.  The Hepatic Microvascular Responses to Sepsis , 2000, Seminars in thrombosis and hemostasis.

[6]  I. Chaudry,et al.  Kupffer cells are responsible for producing inflammatory cytokines and hepatocellular dysfunction during early sepsis. , 1999, The Journal of surgical research.

[7]  J. Crawford CELLULAR AND MOLECULAR BIOLOGY OF THE INFLAMED LIVER , 1997 .

[8]  Z. Ba,et al.  Mechanism of hepatocellular dysfunction during early sepsis. Key role of increased gene expression and release of proinflammatory cytokines tumor necrosis factor and interleukin-6. , 1997, Archives of Surgery.

[9]  L. Hinshaw,et al.  Sepsis/septic shock: participation of the microcirculation: an abbreviated review. , 1996, Critical care medicine.

[10]  T. Billiar,et al.  Liver injury during sepsis. , 1995, Journal of critical care.

[11]  Z. Ba,et al.  HEPATOCELLULAR DYSFUNCTION OCCURS EARLIER THAN THE ONSET OF HYPERDYNAMIC CIRCULATION DURING SEPSIS , 1995, Shock.

[12]  M. Fink,et al.  Laboratory models of sepsis and septic shock. , 1990, The Journal of surgical research.