Abstract
Prostaglandins participate in the pathophysiology of endotoxin shock; however, their exact role has not yet been clear. In this study, we investigated the role of the proaggregatory vasoconstrictor, thoromboxane A2 (T×A2), an arachidonic acid metabolite, during canine endotoxin shock. The central venous plasma levels of thromboxane B2 (T×B2), the stable metabolite of T×A2, was measured by radioimmunoassay. We also investigated the therapeutic effect of reduced glutathione (GSH), a potential cell-stabilizing sulfhydryl compound, in canine endotoxin shock. Sixty minutes after the intraveous administration of E. coli endotoxin (1 mg/kg), the plasma T×B2 levels were significantly increased from 68.8±49.0 pg/ml to 318.3±117.2 pg/ml (N=5) in the control group and from 67.9±68,4 pg/ml to 222.6±133.2 pg/ ml (N=5) in the GSH (300 mg/kg/hr) group. The levels in the GSH group were somewhat lower than in the control group for 60 to 180 minutes after the injection of endotoxin. Thromboxane A2 value appear not to relate to early thrombocytopenia and pulmonary hypertension but to relate to the change of late coagulopathy and of pulmonary vascular resistance. The administration of GSH suppressed the lactic acidemia significantly, however there was a much more decrease in the mean arterial pressure in the GSH group than in the control group. In addition, there was a tendency to inhibit the increase of the serum β-glucronidase activity in the GSH group.
