抄録
Induction of electrical abnormalities(EAs)under simulated ischemic conditions and after reperfusion was measured from single cardiac myocytes isolated from guinea pig ventricle using whole-cell voltage or current clamp with perforated patch variation.Conditions of simulated ischemia were produced by the exchange of medium from the standard one oxygenated with 95%O2−5%CO2 gas(pH7.4)to the modified one, which contained no glucose, 8mM K+ and 30mM sodium-D, L-lactate and was gassed with 90% argon −10%CO2(pH6.6).Under the simulated ischemia for 20min, EAs such as delayed afterdepolarization, early afterdepolarization, automatic activity or transient inward current were observed in about 37% of myocytes driven electrically at 1Hz.Irreversible hypercontracture occurred in myocytes of 10% or less.Upon reperfusion with the standard solution, EAs and hypercontracture were oberved in about 43% and 22% of cells, respectively.Glibenclamide-sensitive current was detected during ischemia, but tended to be enhanced during reperfusion.Amplitude of Ca2+ current and ATP-sensitive K+ current after reperfusion varied widely with time and from cell to cell.When myocytes were pretreated for 10min with 10nM benidipine, a 1, 4-dihydropyridine derivative Ca2+ blocker, the incidence of EAs and hypercontracture was markedly reduced, suggesting the protective effect of benidipine against cardiac cell injury during ischemia and reperfusion.
