Propofol mitigates systemic oxidative injury during experimental cardiopulmonary cerebral resuscitation

Effects of propofol, an intravenous anesthetic agent that exerts potent antioxidant properties, were investigated in an experimental model of cardiac arrest and cardiopulmonary resuscitation. An extended cardiac arrest with 15 randomized piglets was studied to assess the effect of propofol or its solvent intralipid as the control group. Oxidative stress (as measured by a major F2-isoprostane) and inflammation (a major metabolite of PGF2α) were evaluated in addition to the hemodynamic evaluation, protein S-100β and in situ tissue brain damage by immunochemistry at sacrifice after 3 h of reperfusion following cardiac arrest and restoration of spontaneous circulation (ROSC). ROSC increased jugular bulb plasma levels of F2-isoprostane and PGF2α metabolite significantly more in controls than in the propofol-treated group. In situ tissue damage after ischemia-reperfusion was variable among the pigs at sacrifice, but tended to be greater in the control than the propofol-treated group. Propofol significantly reduced an ROSC-mediated oxidative stress in the brain.