Effects of lactate on intracellular pH and hypercontracture during simulated ischemia and reperfusion in cardiac ventricular myocytes of the guinea pig

Effects of lactate on changes in intracellular pH (pH(i)) and contractility during simulated ischemia and reperfusion were examined in single myocytes of the guinea pig cardiac ventricle. The conditions of simulated ischemia were produced by the exchange of perfusion medium from the standard one oxy genated with 95% O-2-5% CO2 gas (pH 7.4) to one containing no glucose, 8 mM K+, and 0-30 mM sodium-D,L-lactate and was gassed with 90% argon-10% CO2 ( pH 6.6). The pH(i) was decreased by the simulated ischemia from approx. 7.3 to approx. 6.9 regardless of lactate concentration, while the rate of pi-I l decrease was increased by lactate in a concentration-dependent manner. Th e contraction induced by electrical stimulation disappeared faster in the p resence of lactate. The incidence of irreversible hypercontracture of myocy tes was significantly reduced by 20-30 mM lactate. The overshoot of pH(i) t o approx. 7.7 and excess contractions were induced by withdrawal of lactate during the reperfusion, but not observed when lactate was continuously pre sent. The recovery of normal contractility during reperfusion was facilitat ed by lactate. It can be concluded that lactate added to or removed from th e perfusion medium increases the rate of pHi change under the simulated isc hemia and reperfusion, respectively, and that the continuous presence of la ctate reduces cell injury under these conditions.