Permissive action of potassium on arrhythmogenesis in the rat heart.
The isolated perfused rat heart was used to assess the influence of extracellular potassium ([K+]0) on vulnerability of the heart to ventricular fibrillation (VF). The VF threshold is reduced when [K+]0 is lowered from 5.9 to 2.0 and 3.0 mmol/l. The vulnerable period is not only widened but VF can be obtained by stimuli on the R wave. The opposite effects are encountered when [K+]0 is increased to 9.0 mmol/l. These alterations in vulnerability to VF are accompanied by an increased incidence of tachyarrhythmias and spontaneous VF during coronary artery ligation and following reperfusion on reduction of [K+]0, with elimination of these arrhythmias on increasing [K+]0 to 9.0 mmol/l. The cellular biochemical responses that accompanied the altered electrical behaviour on alterations of [K+]0 involved the tissue levels of cyclic AMP in both non-ischaemic and ischaemic myocardium and tissue levels of Ca2+ whereas tissue levels of high energy phosphates, adenosine, inosine, hypoxanthine, lactate, Na+, K+ and Mg2+ did not discriminate between hearts vulnerable and hearts resistant to VF. In this model the extracellular K+ level is a determinant of vulnerability to ventricular fibrillation while ischaemic tissue levels of Ca2+ provide the best correlation with alterations in vulnerability.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D002118:Calcium / Q000032:analysis; D003326:Coronary Circulation; D003327:Coronary Disease / Q000150:complications*; D000242:Cyclic AMP / Q000032:analysis; D004198:Disease Susceptibility; D004562:Electrocardiography; D009206:Myocardium / Q000032:analysis; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D014693:Ventricular Fibrillation / Q000209:etiology
D000242:Cyclic AMP; D011188:Potassium; D002118:Calcium