Scientific article
English

Hepatic regeneration is decreased in a rat model of sinusoidal obstruction syndrome

Published in

Journal of surgical oncology, vol. 99, no. 7, p. 439-446

Publication date

2009

Abstract

BACKGROUND AND OBJECTIVES: Oxaliplatin is a chemotherapeutic drug for colorectal adenocarcinoma able to extend the indications for resection of colorectal liver metastases. However, the drug may severely injure hepatic sinusoids, inducing a sinusoidal obstruction syndrome in non-tumoral parenchyma with a risk of decreased regeneration in the remnant liver following partial hepatectomy. METHODS: We then investigated the evolution of hepatic functions and liver regeneration following partial hepatectomy in rats with sinusoidal obstruction syndrome. The sinusoidal obstruction syndrome was induced with a single intragastric administration of monocrotaline (MCT). RESULTS: MCT administration induced obstruction of the hepatic microcirculation and increased portal pressure, hepatic VEGF expression, and Ki67 positive hepatocytes. A mild cholestasis was present without modification of hepatic tests. Following a 70% hepatectomy, liver regeneration was significantly impaired by MCT administration and this impaired regeneration was associated with hepatocellular injury evidenced 1 week after hepatectomy. CONCLUSIONS: The presence of sinusoidal obstruction syndrome impairs hepatic regeneration in this rat model of sinusoidal obstruction syndrome.

Keywords

  • Animals
  • Antineoplastic Agents/adverse effects
  • Colorectal Neoplasms/drug therapy
  • Disease Models, Animal
  • Hepatectomy
  • Hepatic Veno-Occlusive Disease/chemically induced/physiopathology/surgery
  • Liver Regeneration
  • Monocrotaline
  • Organoplatinum Compounds/adverse effects
  • Rats
  • Rats, Sprague-Dawley

Citation (ISO format)

SCHIFFER, Eduardo et al. Hepatic regeneration is decreased in a rat model of sinusoidal obstruction syndrome. In: Journal of surgical oncology, 2009, vol. 99, n° 7, p. 439–446. doi: 10.1002/jso.21276

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Article (Published version)

Identifiers

Journal ISSN

0022-4790
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