IONIC MECHANISMS OF ACTION-POTENTIAL PROLONGATION AT LOW-TEMPERATURE IN GUINEA-PIG VENTRICULAR MYOCYTES

1. We studied the effects of low temperature on the action potentials and membrane currents of guinea-pig ventricular myocytes, using a tigh t-seal whole-cell clamp technique. 2. The action potential duration at 95% repolarization was prolonged from 146 +/- 33 ms (mean +/- S.D., n = 6) at 33-34-degrees-C (control temperature) to 314 +/- 83 ms at 24- 25-degrees-C (low temperature). 3. In whole-cell clamp experiments, lo w temperature decreased the calcium current (I(Ca)), the delayed recti fier potassium current (I(K)), and the inwardly rectifying potassium c urrent (I(K1)) with 'apparent' Q10 (temperature coefficient) values of 2.3 +/- 0.6 for I(Ca), 4.4 +/- 1.2 for I(K) tail current and 1.5 +/- 0.3 for I(K1) (n = 7). 4. The effect of low temperature on I(K) was fu rther studied in the presence of 0.6 muM nicardipine to block I(ca). T he decay phase of the I(K) tail consisted of two exponential component s. The fast but not the slow component was highly sensitive to the tem perature change with an apparent Q10 of 4.5. 5. We found that a compon ent of time-independent current is also sensitive to the temperature. The current had a linear I-V relationship, and remained almost unchang ed after inhibition of Na+-K+ pump in K+-free external solution. 6. Us ing our mathematical model of the ventricular action potential (a modi fication from the DiFrancesco-Noble model), we simulated the action po tential at low temperature by modifying some of the membrane currents, namely I(K), I(K1), I(Ca) and a component of background current. It w as shown that simultaneous changes in these currents could reproduce a pproximately 75% of the action prolongation induced by low temperature .