The aim of the present study was to investigate whether clinical doses of
propofol and
thiamylal affect
oxygen free radical production and intracellular
calcium concentration ([Ca2+]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 [Ca2+]i marker. The hearts were divided into 6 groups as follows (each group: n = 8); Group S (saline), Group TL (
thiamylal 100 microM), Group TH (
thiamylal 300 microM), Group I (
Intralipid), Group PL (
propofol 3 microM), and Group PH (
propofol 10 microM). 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 [Ca2+]i were observed in all groups except Group TH. The high dose of
thiamylal significantly suppressed this initial increase in cytosolic [Ca2+]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 [Ca2+]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 [Ca2+]i before and after
ischemia, whereas
thiamylal suppressed the increase in [Ca2+]i during
ischemia and reperfusion. However,
free radical formation during reperfusion was unaffected by
thiamylal and
propofol.