The effect of propofol on oxidative stress in platelets from surgical patients.

UNLABELLED: We investigated the changes in oxidative stress in platelets from surgical patients anesthetized with propofol. We studied 60 surgical patients (ASA physical status I and II) and 12 healthy volunteers. The patients were divided into three groups: anesthesia induced with an IV bolus dose of 4 mg/kg thiopental; anesthesia induced with an IV bolus dose of 2 mg/kg propofol; and total IV anesthesia (induction with propofol 2 mg/kg, infusion with propofol 10 mg/kg during the first 10 min, then 8 mg/kg for 10 min, and 6 mg/kg during the rest of the operation). Healthy volunteers were given an IV bolus dose of 10% fat emulsion (Intralipid). We measured the following variables in platelets: thiobarbituric acid reactive substances content, glutathione content, and glutathione peroxidase, reductase, and transferase activities. Thiopental did not modify any of the variables. Propofol decreased thiobarbituric acid reactive substances production by 25.7% and increased total glutathione content by 24.6%. The percentage of glutathione in oxidized form was 29.5% smaller in patients anesthetized with propofol. Glutathione peroxidase activity was 28.3% less, glutathione transferase was 44.5% more, and glutathione reductase was not significantly different. Intralipid had no effect on any of the variables. After infusion of propofol for 1 h, the effects were, in qualitative terms, the same as those seen after an initial bolus dose. In conclusion, our findings show that propofol has an antioxidant effect in humans. This effect may be beneficial in patients who have diseases in which free radicals play an important role. IMPLICATIONS: This study demonstrates that propofol inhibits cellular oxidative damage, measured in platelets from surgical patients. Neither thiopental nor the fat emulsion (Intralipid) showed any effect. Moreover, propofol increased the antioxidant defense of glutathione. This could be applied in the protection of tissues from ischemic damage.