Recently it has been shown that during liver ischemia at 25 degrees C the presence of glycogen, by supporting glycolytic supply, not only retards ATP decay but also leads to a corresponding delay of the rise of the electrical impedance of the ischemic organ. A sudden rise of impedance during ischemia is supposed to indicate the closure of gap junctions. Although similar effects on energy state do exist at low temperature, the impact of glycogen on the electrical impedance under storage conditions has still to be evaluated. Therefore, in a model with protected porcine livers, we examined the intraischemic effects of a preischemic glucose and potassium feeding on impedance changes, lactate production and ATP-content at a storing temperature of 5 degrees C. Impedance was measured both in the low frequency alpha- and the higher frequency beta-dispersion range. In addition, the same parameters were determined in a group of unprotected livers. In this group all animals had received glucose and potassium orally prior to ischemia. Whereas in case of preischemic glucose feeding the rise of impedance in the range of the beta-dispersion (e.g. 5kHz) roughly coincided with the exhaustion of ATP, the corresponding impedance changes in the protected group without a glucose premedication only occurred when glycolysis had already stopped and ATP had reached basal values for some hours. In contrast, in the alpha-dispersion range the impedance changes in the latter group just began at the time when ATP became exhausted and lactate production ceased.(ABSTRACT TRUNCATED AT 250 WORDS)