Plegisol with added sodium bicarbonate when cooled and instilled into the coronary artery vasculature, causes prompt arrest of cardiac electromechanical activity, combats intracellular ion losses and buffers ischemic acidosis. When used with hypothermia and ischemia, the action may be characterized as cold ischemic potassium-induced cardioplegia. This is conducive to providing the surgeon with a quiet, relaxed heart and bloodless field of operation.
Calcium (Ca++) ion in low concentration is included in the solution to maintain integrity of cell membrane to ensure that there is no likelihood of calcium paradox during reperfusion.
Magnesium (Mg++) ion may help stabilize the myocardial membrane by inhibiting a myosin phosphorylase, which protects adenosine triphosphate (ATP) reserves for postischemic activity. The protective effects of magnesium and potassium have been shown to be additive.
Potassium (K+) ion concentration is responsible for prompt cessation of mechanical myocardial contractile activity. The immediacy of the arrest thus preserves energy supplies for postischemic contractile activity in diastole.
The chloride (Cl‾) and sodium (Na+) ions have no specific role in the production of cardiac arrest. Sodium is essential to maintain ionic integrity of myocardial tissue. The chloride ions are present to maintain the electroneutrality of the solution.
Added bicarbonate (HCO3‾) anion is included as a buffer to render the solution slightly alkaline and compensate for the metabolic acidosis that accompanies ischemia.
Extemporaneous alternative buffering to the described formulation of this solution is not recommended.