This study investigates the plasma levels of 8-iso-PGF PK , a non-enzymatic, and 15-K-DH-PGF PK , a cyclooxygenase catalyzed oxidation product of arachidonic acid in an experimental porcine endotoxemic shock model. A significant (P 6 0.001) and rapid appearance and disappearance of PGF PK metabolite after endotoxin infusion was very similar in both nonsurvival and survival groups indicating an acute progression and recession of inflammation. When oxidative injury was assessed by measuring free 8-iso-PGF PK 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-PGF PK 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.z 1998 Federation of European Biochemical Societies.
Endotoxemia in the pig rapidly induced hypocalcemia. Calcium accumulation was found in ascites and in the liver, but not in other examined tissues. Calcium administration, restoring the Ca2+ concentration, did not improve hemodynamics or survival in this model of hypodynamic sepsis. Porcine endotoxemic shock, which replicates human septic shock, seems to be suitable for evaluating calcium turnover.
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