<Original Article> Inhibitory Effects of Propofol on Hydrogen-Peroxide Induced Oxidative Injury in Mouse Myocytes

The effects of 10-5 M propofol or its solvent, intralipid on intracellular Ca2+ concentration ([Ca2+]i) and beating rate were studied in cultured mouse fetal myocytes exposed to hydrogen peroxide (H2O2) using a Ca2+-sensitive fluorescent dye, indo-1. The peak systolic and diastolic levels of [Ca2+]i in the cultured myocytes were 1823±317 nM and 557±300 nM, respectively (n=24). Propofol, 10-5 M, decreased the peak systolic [Ca2+]i and beating rate significantly compared with those before propofol administration (p<0.001 for both systolic [Ca2+]i and beating rate). The myocytes exposed to H2O2 showed decreases in the peak systolic [Ca2+]i and beating rate. Diastolic [Ca2+]i were unchanged before the cessation of spontaneous beating. Around 10 min after the H2O2 exposure, spontaneous beating stopped and [Ca2+]i began to increase. In the myocytes exposed to H2O2 with propofol, the time before the cessation of spontaneous beating was significantly longer than that in either the myocytes exposed only to H2O2 or those exposed to H2O2 with intralipid (p<0.05 for H2O2 and H2O2 with intralipid). Moreover, [Ca2+]i in the myocytes exposed to H2O2 with propofol was significantly lower when compared with those of the H2O2 without propofol at 5 min after cessation of spontaneous beating (p<0.05). These results demonstrate that propofol can delay the cessation of spontaneous beating and attenuate excessive intracellular Ca2+ accumulation induced by exogenous H2O2. The mechanisms of these effects of propofol may be related to L-type Ca2+ channel blocking and antioxidant effects.