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Histopathologic Study of Cholestasis Induced by Total Parenteral Nutrition or Intraperitoneal Sepsis in Rats
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Wistar rats were divided into two groups, intraperitoneal sepsis group (group IS) and total parenteral nutrition group (group TPN), to evaluate the characteristics of pathologic alterations in rats with cholestasis. Biochemical assay showed that cholestasis developed in both groups after 10 days. Light microscopic examination of liver specimens revealed that the degeneration in the intermediate and external zone of hepatolobules was the major alteration in group IS, and group TPN showed characteristic dilation of central veins and hepatic sinuses and the proliferation of Kupffer cells with marked phagocytosis. Electron microscopic pictures presented the enlargement of bile canaliculi with altered microvilli in group IS and many highly electron‐dense bile particles within cytoplasm and secondary lysosomes near dilated bile canaliculi in group TPN. It is concluded that there were different histopathologic alterations of liver specimens in TPN‐supported animals and septic animals when cholestasis developed. It is unsuitable to take intraperitoneal sepsis as a unique factor of cholestasis in TPN‐supported rats. Bile stasis is only one sign of TPN‐induced hepatic lesion, which needs further exploration to determine its causes and mechanisms. (Journal of Parenteral and Enteral Nutrition 15:630–636, 1991)
Title: Histopathologic Study of Cholestasis Induced by Total Parenteral Nutrition or Intraperitoneal Sepsis in Rats
Description:
Wistar rats were divided into two groups, intraperitoneal sepsis group (group IS) and total parenteral nutrition group (group TPN), to evaluate the characteristics of pathologic alterations in rats with cholestasis.
Biochemical assay showed that cholestasis developed in both groups after 10 days.
Light microscopic examination of liver specimens revealed that the degeneration in the intermediate and external zone of hepatolobules was the major alteration in group IS, and group TPN showed characteristic dilation of central veins and hepatic sinuses and the proliferation of Kupffer cells with marked phagocytosis.
Electron microscopic pictures presented the enlargement of bile canaliculi with altered microvilli in group IS and many highly electron‐dense bile particles within cytoplasm and secondary lysosomes near dilated bile canaliculi in group TPN.
It is concluded that there were different histopathologic alterations of liver specimens in TPN‐supported animals and septic animals when cholestasis developed.
It is unsuitable to take intraperitoneal sepsis as a unique factor of cholestasis in TPN‐supported rats.
Bile stasis is only one sign of TPN‐induced hepatic lesion, which needs further exploration to determine its causes and mechanisms.
(Journal of Parenteral and Enteral Nutrition 15:630–636, 1991).
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