Regional Increase in Extracellular Potassium Causes Arrhythmias in Rat Cardiac Muscle

Background: Extracellular potassium ([K⁺]_o) increases to >20 mM in the ischemic myocardium. We investigated whether this regional increase in [K⁺]_o affects arrhythmias. Methods: To produce a, regional, increase in [K⁺]_o (K_R), rat trabeculae were regionally exposed to a jet of solution containing 30 mM KCl. To produce a global, increase in [K⁺]_o (K_G), trabeculae were superfused with a solution containing 30 mM KCl. Force, sarcomere length, membrane potential, and [Ca²⁺]i were measured (24°C, [Ca²+]_o=3.0 mM). The velocity (V_prop) and amplitude (CaCW) of Ca²⁺ waves were measured. Results: K_R caused nonuniform contraction and increased the V_prop and Ca_cw, while K_G decreased the Ca_cw. The increase in the Ca_cw with K_R was not suppressed by 100 μM streptomycin, while it was suppressed by 1) both 10 μM cilnidipine and 3 μM SEA0400, 2) 20 mM 2,3-butanedione monoxime, and 3) 10 μM blebbistatin. With 200 nM isoproterenol, K_R induced sustained arrhythmias (>10 s), while K_G induced no sustained arrhythmias. During sustained arrhythmias with K_R, Ca²⁺ surged within the border zone (BZ) around the jet-exposed region and were succeeded by synchronous increases in [Ca²⁺]i. Stoppage of the jet caused the Ca²⁺ surge to become unclear and resulted in the arrest of sustained arrhythmias. Conclusions: A regional but not global increase in [K⁺]_o induces sustained arrhythmias, probably due to nonuniform contraction.