SUMMARYThe aim of the present study was to investigate whether clinical doses of propofol and thiamylal affect oxygen free radical production and intracellular calcium concentration ([Ca 2+ ] i ) in the post-ischemic reperfused heart. Forty-eight rat hearts were perfused with a Langendorff system and loaded with Fura-2 / AM as a [Ca 2+ ] i marker. The hearts were divided into 6 groups as follows (each group: n = 8); Group S (saline), Group TL (thiamylal 100 µM), Group TH (thiamylal 300 µM), Group I (Intralipid), Group PL (propofol 3 µM), and Group PH (propofol 10 µM). All hearts were initially perfused for 5 min as control aerobic perfusion. Afterwards, no-flow ischemia was induced for 15 min, followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent was measured with high performance liquid chromatography using salicylic acid. At the beginning of the ischemia and reperfusion periods, increases in systolic and diastolic [Ca 2+ ] i were observed in all groups except Group TH. The high dose of thiamylal significantly suppressed this initial increase in cytosolic [Ca 2+ ] i (Group S 1.30 ± 0.15; Group TL 0.99 ± 0.17; Group TH 0.70 ± 0.09, at 1 min after reperfusion; systolic [Ca 2+ ] i : p < 0.05). Total DHBAs in the coronary effluent of all groups increased significantly 1 min after reperfusion, however, there were no significant differences among the groups. Clinical doses of propofol had no significant effect on myocardial function and [Ca 2+ ] i before and after ischemia, whereas thiamylal suppressed the increase in [Ca 2+ ] i during ischemia and reperfusion. However, free radical formation during reperfusion was unaffected by thiamylal and propofol. (Jpn Heart J 2001; 42: 193-206) Key words: Heart, Hydroxyl radical, Intracellular calcium concentration, Propofol, Thiamylal PROPOFOL (2,6-diisopropylphenol) is widely used for the induction and maintenance of anesthesia because of its quick onset of action and its favorable pharmacokinetic profile for early emergence after discontinuation of an intravenous administration. The cardiovascular effects of propofol include decreases in arterial pressure as a result of reduced cardiac output and peripheral vasodilation.