Oxidative injury and survival during endotoxemia.
This study investigates the plasma levels of 8-iso-PGF2alpha, a non-enzymatic, and 15-K-DH-PGF2alpha, a cyclooxygenase catalyzed oxidation product of arachidonic acid in an experimental porcine endotoxemic shock model. A significant (P < 0.001) and rapid appearance and disappearance of PGF2alpha metabolite after endotoxin infusion was very similar in both non-survival and survival groups indicating an acute progression and recession of inflammation. When oxidative injury was assessed by measuring free 8-iso-PGF2alpha the levels in plasma increased significantly up to 2 h and remained at this level until death among the non-survivors. This was apparently different from the survivors where the 8-iso-PGF2alpha levels increased to its height at 1 h, then decreased to the basal levels after 5 h. Thus, free radical and cyclooxygenase catalyzed oxidation of arachidonic acid occurs during endotoxemia. Free radical dependent oxidative injury following endotoxin induced inflammation may be the major cause of organ failure and increased mortality.
Basu
S
S
Department of Geriatrics, Faculty of Medicine, Uppsala University, Sweden. samar.basu@geriatrik.uu.se
Eriksson
M
M
D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000097:blood; D019446:Endotoxemia / Q000401:mortality / Q000503:physiopathology*; D004927:Escherichia coli Infections / Q000097:blood / Q000401:mortality / Q000503:physiopathology; D028441:F2-Isoprostanes; D005260:Female; D007249:Inflammation; D008297:Male; D018384:Oxidative Stress; D011863:Radioimmunoassay; D012772:Shock, Septic / Q000097:blood* / Q000401:mortality / Q000503:physiopathology; D016019:Survival Analysis; D013552:Swine; D013997:Time Factors
D015415:Biomarkers; D028441:F2-Isoprostanes; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; C075750:8-epi-prostaglandin F2alpha; D016718:Arachidonic Acid; D015237:Dinoprost