Imidazole-buffered cardioplegic solution. Improved myocardial preservation during global ischemia

Progressive acidosis is a constant finding in global myocardial ischemia and is associated with reduced myocardial contractility after ischemia. The hypothesis tested in these experiments was that imidazole (pKa = 6.7 at 37 degrees C), a commonly used buffer in physiology and microbiology, would provide superior buffering capacity when used in lieu of bicarbonate (pKa = 6.1 at 37 degrees C) in a cardioplegic solution. Twenty-eight isolated, working rabbit hearts were perfused, and preischemic and postischemic determinants of performance were measured. The 30 minute interval of normothermic global ischemia was altered by the injection at 0 and 15 minutes of 2 ml/gm wet weight of a buffered cardioplegic solution. Control hearts received a bicarbonate-buffered cardioplegic solution and experimental hearts received a solution buffered with imidazole. In the imidazole-buffered group, there was a superior recovery of coronary flow, developed left ventricular pressure, peak rate of rise of left ventricular pressure, peak rate of relaxation, and stroke work indices (p less than 0.05). Recovery of mechanical parameters was coincident with an improved acid-base status of the coronary sinus effluent at the end of ischemia. Coronary sinus effluents in the imidazole group had significantly higher pH values and lower partial pressures of carbon dioxide than coronary sinus effluents in the bicarbonate-buffered group (p less than 0.001). The data suggest that improved buffering of the extracellular and possibly intracellular space during global ischemia with a nonbicarbonate buffer is beneficial and provides improved postischemic myocardial recovery.