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An experimental study was undertaken to study the influences of an infusion of lipid emulsion on phagocytosis of Kupffer's cells in septic rats. Sepsis was induced in 13 rats by ligating the cecum. Five of them received glucose as the sole nonprotein calorie (septic-glucose group), four of the rats received 25% of the nonprotein calorie with lipid emulsion, Intralipid (septic-lipid group), and the remaining four rats did not receive any intravenous solution and were allowed access to water (septic-fasted group). Another four rats which received neither intravenous solution nor ligation of the cecum served as the control group. The intravenous infusion was carried out for 72 hr. The phagocytotic activity of Kupffer's cells was determined by the ability to engulf latex particles with a size of 1.09 micron, in vitro. The phagocytotic activity was enhanced by the presence of sepsis but it was inhibited by starvation. The difference in the phagocytotic activity between the septic-glucose group and the septic-lipid group was not significant. These results suggest that, insofar as an in vitro study is concerned, a 72-hr infusion of lipid emulsion at a rate of 25% of the total nonprotein calorie does not influence the phagocytotic activity of cultured Kupffer's cell obtained from septic rats.

The effects of parenteral nutrition (PN) and of the difference in the PN regimens between glucose and lipid emulsion on the development of endogenous endotoxemia were studied in 40 Wister rats. Endotoxemia was induced by occluding the superior mesenteric vein (SMV) for 30 min. The plasma endotoxin in the portal blood at the time of the release of the SMV occlusion and that in the arterial blood 10 min after the release were quantified. Twenty of the 40 rats had received PN for 48 hr prior to the SMV occlusion. Ten of these 20 rats received the total nonprotein calorie (TNPC) solely with glucose, and the other 10 rats received 25% of the TNPC with lipid emulsion. Ten rats had been allowed free access to lab food until the SMV occlusion. The remaining 10 rats underwent neither the SMV occlusion nor PN, and served as the control group. Both the portal and the arterial endotoxin increased after the release of the SMV occlusion, however the portal endotoxin was higher than that of the arterial one. Both the portal and the arterial endotoxin of the rats supported by PN were significantly lower than those of the rats nourished by lab food, while they were higher than the control values. The difference in the PN regimens did not cause any alteration in the endotoxin levels. These results indicate that the development of intestinal endotoxemia was not influenced by the difference in the PN regimens, but it was rather influenced by a presence of intestinal content.