Studies of cat heart muscle during recovery after prolonged hypothermia. Hyperpolarization of cell membranes and its dependence on the sodium pump with electrogenic characteristics.

Cat heart muscles preserved in normal Tyrode's solution at 4°C for prolonged periods were investigated by recording the transmembrane potentials after rewarming to 37°C. The cell membranes were gradually hyperpolarized during rewarming, the maximum hyperpolarization being reached within a few hours. The amplitude of resting potentials obtained at a maximally hyperpolarized stage was largest for ventricular muscle that had been preserved for 20 hours at 4°C and for atrial muscle that had been preserved for about 50 hours at 4°C. The maximum potentials averaged 267.7 mv for the ventricles and 184.4 mv for the atria. KC1 at 10 X normal and epinephrine and norepinephiine in final concentrations of 2.5 X 10~ g/ml brought about a marked hyperpolarization of the cell membrane when the membrane potential of the muscles was declining. The cells of muscles loaded with Li had a greater than normal membrane potential for an hour during gradual equilibration over a range of 4 to 22°C before rewarming. When muscles were rewarmed to 37°C in Li-Tyrode's solution the membrane potential gradually decreased to 5 to 23 mv for the right atrium and 13 to 34 mv for the right ventricle. Ouabain 10~ and 10"c M abolished the hyperpolarization and subsequently depolarized the cell membrane. DNP (0.2 and 0.6 ITIM) and sodium azide (6 HIM) also had an inhibiting effect on the hyperpolarization. The observations are consistent with a hypothesis of an electrogenic sodium pump, which produces hyperpolarization whose magnitude depends largely on the previous length of time the tissue was preserved in the hypothermic state. ADDITIONAL