The role of Kupffer cells in the development of hepatic dysfunction during sepsis.

The effect of Kupffer cell blockade on hepatic function during sepsis was evaluated in this study. Methyl palmitate suspension 100 mg/100 g administered intravenously suppressed the phagocytic activity as the phagocytic index K decreased from 0.0493 +/- 0.0089 to 0.0150 +/- 0.0035 in rats. Sepsis was produced by the method of cecal ligation and needling perforation (CLP). At the end of 15 hours after CLP the hepatic adenosine triphosphate (ATP) level and ketone body ratio decreased significantly. But in rats pretreated with methyl palmitate 24 hours prior to CLP, the ATP level returned to the normal control level (1.6906 +/- 0.06-2.2323 +/- 0.13 mumol/g) and ketone body ratio remained at significantly higher values (0.26 to 0.68). After CLP, the liver lipoperoxide (LPO) concentration increased and glutathione (GSH) contents decreased significantly. When the septic rats were pretreated with methyl palmitate, both the LPO and GSH returned to the normal control level (62.69 +/- 1.7 to 44.62 +/- 2.12 and 159.85 +/- 9.7 to 222.27 +/- 11.34). It is concluded that the hepatic dysfunction is modulated at least to a greater extent by many of the toxic mediators released by the activated Kupffer cells during sepsis.

The role of Kupffer cells in the development of hepatic dysfunction during sepsis.

The effect of Kupffer cell blockade on hepatic function during sepsis was evaluated in this study. Methyl palmitate suspension 100 mg/100 g administered intravenously suppressed the phagocytic activity as the phagocytic index K decreased from 0.0493 +/- 0.0089 to 0.0150 +/- 0.0035 in rats. Sepsis was produced by the method of cecal ligation and needling perforation (CLP). At the end of 15 hours after CLP the hepatic adenosine triphosphate (ATP) level and ketone body ratio decreased significantly. But in rats pretreated with methyl palmitate 24 hours prior to CLP, the ATP level returned to the normal control level (1.6906 +/- 0.06-2.2323 +/- 0.13 mumol/g) and ketone body ratio remained at significantly higher values (0.26 to 0.68). After CLP, the liver lipoperoxide (LPO) concentration increased and glutathione (GSH) contents decreased significantly. When the septic rats were pretreated with methyl palmitate, both the LPO and GSH returned to the normal control level (62.69 +/- 1.7 to 44.62 +/- 2.12 and 159.85 +/- 9.7 to 222.27 +/- 11.34). It is concluded that the hepatic dysfunction is modulated at least to a greater extent by many of the toxic mediators released by the activated Kupffer cells during sepsis.