Figure 2.

The cellular targets for hyperpolarized/polarized arrest.Adenosine-related cardioplegic effect arises from the inhibition of the sino-atrial and atrioventricular nodes, as well as from the activation of A1 receptors located on atria and ventricular cells, which open sarcolemma KATP channels to reduce action potential duration. KCO’s allows an increased potassium flux through the sarcolemma that will shift membrane potential towards the K⁺ equilibrium potential, which is normally around −90 mV in myocytes. Local anesthetic agents block the voltage-gated Na+ fast channels that are responsible for the action potential upstroke, thereby maintaining the membrane potential at/around its resting value. Ca-antagonist agents inhibit the L-type calcium channels, thus inhibiting the smooth muscle cell’s contractility.