Effects of three intravenous lipid emulsions on the survival and mononuclear phagocyte function of septic rats.
The immunosuppressive effects of intravenous lipid emulsions are a matter of great concern and debate. In a rat model of gram-negative bacteremia, we assessed whether the use of three intravenous lipid emulsions with different triacylglycerol compositions could influence mortality, bacterial clearance, and prostaglandin E(2) (PGE(2)) levels and compared these groups with groups of orally fed rats and rats that received a small amount of calories in form of glucose without enteral feeding (starvation). RATS WERE ASSIGNED TO ONE OF FIVE GROUPS: group 1 (control, n = 15) received rodent chow ad libitum and saline infusion; group 2 (starvation group, n = 12) had no access to chow and received an infusion of 5% glucose; group 3 (n = 17) received total parenteral nutrition (TPN) with long-chain triacylglycerols; group 4 (n = 12) received TPN with medium- and long-chain triacylglycerols; and group 5 (n = 15) received TPN with its emulsion based on olive oil. Animals received isonitrogenous and isocaloric TPN. After 2 d of TPN, a dose of 10(8) colony-forming units of Escherichia coli was introduced via the venous catheter; 2 d later the animals were killed. Blood, spleen, liver, and lungs were cultured. Circulating levels of PGE(2) were measured. Bacterial growth in the liver and lungs were significantly higher in groups 3 and 4 than in group 1, with no differences among the other groups. Rates of bacteremia were significantly higher in groups 3 and 4 than in group 1, with no differences among the other groups. Plasma levels of PGE(2) did not differ, and mortality was unaffected. Bacterial clearance clearly was preserved in orally fed, control rats when compared with rats on TPN with long-chain triacylglycerols or medium- plus long-chain triacylglycerols. However, the use of a lipid emulsion enriched intravenously with oleic acid was a valid way of reducing this disturbance, although plasma levels of PGE(2) and survival were not modified.
Garnacho-Montero
J
J
Intensive Care Unit, Hospital Universitario Virgen del Rocío, Seville, Spain. jgmrji@arrakis.es
Ortiz-Leyba
C
C
Garnacho-Montero
M C
MC
Garcia-Garmendia
J L
JL
Pérez-Paredes
C
C
Moyano-Del Estad
M R
MR
Barrero-Almodóvar
A
A
Jiménez-Jiménez
F J
FJ
D000284:Administration, Oral; D000818:Animals; D016470:Bacteremia / Q000276:immunology / Q000401:mortality / Q000628:therapy; D015169:Colony Count, Microbial; D015232:Dinoprostone / Q000097:blood*; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000254:growth & development / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology / Q000401:mortality / Q000628:therapy; D005217:Fat Emulsions, Intravenous / Q000008:administration & dosage* / Q000009:adverse effects; D008099:Liver / Q000382:microbiology; D008168:Lung / Q000382:microbiology; D008297:Male; D010289:Parenteral Nutrition, Total; D010586:Phagocytes / Q000187:drug effects* / Q000276:immunology / Q000502:physiology; D010587:Phagocytosis / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000276:immunology / Q000401:mortality / Q000628:therapy*; D014280:Triglycerides / Q000008:administration & dosage
D005217:Fat Emulsions, Intravenous; D014280:Triglycerides; D015232:Dinoprostone