A conventional (single sucrose gap) voltage clamp technique was employed to investigate the rate dependence of ionic currents activated in the plateau range of potential in the rabbit ventricular muscle. A transient outward current of increasing amplitude was observed when the period of rest preceding the test voltage clamp pulse was increased from 0.7-60 s. The action potential duration was short when the transient outward current peak (100-150 ms after the voltage clamp pulse beginning) was high under the studied conditions of stimulation (interbeat intervals 0.7-60 s). The rate dependent transient outward current was small at low levels of depolarization above the resting potential (40 mV), had a maximum at some 90-100 mV and decreased at more positive potentials. This current was sensitive to the simultaneous application of 4-aminopyridine and calcium substitution with strontium in the Tyrode solution. It is suggested that the transient outward current is probably responsible for the changes of the action potential duration in rabbit papillary muscles when the interbeat interval varies from some 0.7-60 s.

In summary, our data suggest that prolonged chronic alcohol consumption for 6 months resulted in increased autolysis of μ-calpain in rat skeletal muscles. These changes were accompanied by reduced titin and nebulin contents, titin hyperphosphorylation, and development of hindlimb muscle atrophy in the alcohol-fed rats.

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The conventional microelectrode technique was used to investigate the effect of long periods of rest (greater than 10s) on the action potential duration of mammalian ventricular muscle. The action potential duration increased as the rest period increased. This prolongation of the action potential was the greatest and the slowest in rabbit ventricle, was smaller and more rapid in guinea-pig ventricle, and was practically absent in rat ventricle. The prolongation of the action potential at rest was suppressed with aminazine and strophanthin. Low sodium concentration, lanthanum ions, ruthenium red and acidosis failed to suppress the slow prolongation. It is concluded that the slow prolongation of the action potential at rest is related to changes in the intracellular calcium content induced by a mechanism different from Na/Ca exchange.

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