Effect of ibuprofen on fever and metabolic changes induced by continuous infusion of leukocytic pyrogen (interleukin 1) or endotoxin

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Abstract
The ability of febrile response-blocking levels of ibuprofen, a specific cyclooxygenase inhibitor, to alter protein and trace metal responses to leukocytic pyrogen or endotoxin [Salmonella enteritidis]. In guinea pigs given continuous infusions of leukocytic pyrogen or endotoxin, a 0.6.degree.-0.8.degree. C fever was observed within 4 h; Zn and Fe concentrations in serum fell by 63-78% (P < 0.01). Rates of whole body amino acid appearance, oxidation and incorporation into protein were all significantly increased by leukocytic pyrogen and endotoxin treatment (P < 0.05), as were the fractional hepatic and seromucoid protein protein synthesis rates in leukocytic pyrogen-treated animals (P < 0.01). Muscle protein synthesis was unchanged. Although pretreatment with infusions of ibuprofen completely ablated the febrile response to leukocytic pyrogen and endotoxin, decreases in Zn and Fe concentrations in serum and leukocytosis were unaffected. Overall increases in whole body amino acid kinetics induced by leukocytic pyrogen or endotoxin were only minimally affected by ibuprofen. Thus, treatment with prostaglandin synthesis inhibitor ibuprofen did not affect whole body trace metal, hematological or hepatic acute-phase-induced responses to leukocytic pyrogen or endotoxin, either because these responses are prostanoid independent or because they are only partially mediated by eicosanoid products. [Ibuprofen administration does not appear to alter the purported beneficial responses to an infection or endotoxin.].