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Lipid peroxidation induced by an early inflammatory response in endotoxaemia
Author(s) -
Basu S.,
Eriksson M.
Publication year - 2000
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.2000.440104.x
Subject(s) - prostaglandin f2alpha , lipid peroxidation , medicine , arachidonic acid , prostaglandin , endocrinology , shock (circulatory) , cyclooxygenase , septic shock , oxidative stress , biochemistry , enzyme , chemistry , sepsis
Background: Endotoxaemic challenge promptly causes lipid peroxidation. Porcine endotoxaemia can be used to replicate severe human septic shock. This model was used to evaluate non‐enzymatic [8‐Iso‐prostaglandin F 2α (8‐Iso‐PGF 2α )] and enzymatic [15‐keto‐13,14‐dihydro‐prostaglandin F 2α (15‐K‐DH‐PGF 2α )] lipid peroxidation, respectively, in relation to survival. The aim of this study was to correlate, if possible, pathophysiologic events during endotoxaemia to the levels of these arachidonic acid metabolites. Methods: Nineteen pigs were anaesthetised, monitored (circulatory and respiratory variables in relation to lipid peroxidation) and given a continuous 6 h E. coli endotoxin (10 μg · kg −1 · h −1 ) infusion. All animals were mechanically ventilated at constant tidal volumes and the inspired oxygen fraction was kept constant during the experimental period. Results: This endotoxin infusion caused expressed derangements in all pigs and death in 9 of them. The levels of 8‐Iso‐PGF 2α , indicating oxidative injury, were different in time course, magnitude and fashion between survivors and non‐survivors. The levels of 15‐K‐DH‐PGF 2α , indicating inflammatory response, showed a similar pattern. At 1 h the CO 2 partial pressure in arterial blood was significantly higher in non‐surviving pigs and correlated (r: 0.7; P <0.05) to the levels of 15‐K‐DH‐PGF 2α . Prostaglandin F 2α is mainly metabolised in the lung. The lung weights were significantly ( P <0.05) higher in non‐surviving than in surviving animals. Both free radical and cyclooxygenase catalysed oxidative modification occurs during endotoxaemia. Conclusion: Increased metabolism and inflammation, as evaluated by 15‐K‐DH‐PGF 2α , in the group of non‐survivors may mediate the increase in arterial CO 2 . Thus, increased lipid peroxidation seems to be associated with endotoxaemic organ dysfunction and increased mortality.