Abstract
It has been suggested that phospholipase A2 (PLA2) plays an important role in the development of shock in patients with endotoxemia. The PLA2 activity was reported to be elevated in the serum of patients with endotoxin shock. To determine the origin and mechanism of the elevated PLA2 activity, we made an endotoxin shock model in rats by injecting 5 mg of lipopolysaccharide (LPS) per kg, intravenously. Serum PLA2 activity increased from 194±25 to 359±56 pmol/ml/min (mean±SEM) 30min after the LPS injection. The PLA2 activity in the liver homogenates also increased from 7.8±0.6 to 10.2±0.2 pmol/mg protein/min after 30min. The increased PLA2 activity was shown to be heat labile and calcium-ion dependent. Ultrastructural enzymehistochemically, PLA2 activity was found in the lysozome membrane of damaged hepatocytes and Kupffer's cells. These results suggest that the increase in heat labile and calcium-ion dependent PLA2 activity is related to tissue damage in the endotoxin shock model.
