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Guinea pig right atria were perfused in vitro at 30°C. When the temperature was lowered to about 20°C, atrial activity ceased and the resting potential of atrial fibers decreased significantly. When activity was restored during hypothermia by electrical stimulation, both the resting and the action potentials were similar to those recorded at 30°C. Blockade of receptors by atropine or propranolol reduced the effects of electrical stimulation on the membrane potentials, and the reduction was greatest when both drugs were present. In particular, propranolol reduced the amplitude of the action potential. Strophanthidin also reduced the increment in resting potential induced by electrical stimulation at low temperature. Norepinephrine restored atrial activity, but the action potential and its rate of rise were small and the resting potential remained low. We concluded that (1) electrical stimulation restored atrial activity by simultaneously depolarizing the membrane to threshold, liberating autonomic mediators, and stimulating the sodium-potassium pump and (2) norepinephrine removed the sinoatrial block induced by low temperature by increasing the slow calcium and sodium currents.

Restoration of Electrical Activity of Guinea Pig Atria during Hypothermia: EFFECTS OF NOREPINEPHRINE AND ELECTRICAL STIMULATION ON MEMBRANE POTENTIALS