Effect of enteral versus parenteral nutrition on inflammation and cardiac function in a rat model of endotoxin-induced sepsis.
The present study examined whether total enteral nutrition (TEN) and total parenteral nutrition (TPN) differentially modulates ghrelin, inflammatory mediator production, and cardiac dysfunction induced by LPS. Rats received isocaloric parenteral or enteral nutrition through implanted vascular catheters or gastrostomy tubes for 7 days. Enteral nutrition was provided in conventional (TEN-C) and immunonutrition (TEN-I) formulations. Subsequently, rats were injected i.v. with LPS. Serum ghrelin, TNF-alpha, and high mobility group box 1 levels were determined by enzyme-linked immunosorbent assay. Myocardiac function was also assessed via the Langendorff isolated heart technique. The TEN-C increased plasma ghrelin and inhibited inflammatory mediators both before and after LPS administration when compared with TPN or TEN-I. Furthermore, animals receiving TPN and TEN-I had significantly lower left ventricular developed pressure but increased pressure development during isovolumetric contraction (dP/dt(max)) and relaxation (dP/dt(min)) when compared with animals receiving TEN-C after LPS-induced shock (P < 0.05). We conclude that TEN-C more effectively increased plasma ghrelin levels than TPN and TEN-I. The maintenance of higher ghrelin levels in TEN-C rats was associated with inhibiting various inflammatory mediators and maintaining cardiac function during LPS-induced septic shock.
Hagiwara
Satoshi
S
Department of Brain and Nerve Science, Anesthesiology, Oita University Faculty of Medicine, Yufu City, Oita, Japan. saku@med.oita-u.ac.jp
Iwasaka
Hideo
H
Shingu
Chihiro
C
Noguchi
Takayuki
T
D000818:Animals; D004195:Disease Models, Animal; D004731:Endotoxins / Q000378:metabolism*; D004750:Enteral Nutrition; D054439:Ghrelin / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000502:physiology; D007249:Inflammation; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D010288:Parenteral Nutrition; D051381:Rats; D018805:Sepsis / Q000473:pathology* / Q000628:therapy*; D012772:Shock, Septic / Q000628:therapy; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D004731:Endotoxins; D054439:Ghrelin; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha