AMINOSULFONIC ACID BUFFER PRESERVES MYOCARDIUM DURING PROLONGED ISCHEMIA

Prevention of myocardial acidosis during global ischemia in operative cardiopreservation was explored in two series of dogs where acid-base control was the only variable. A specifically designed aminosulfonic a cid buffer composition, 3:1 molar equivalents NaMOPS to HEPES, 0.2 mol /L, was compared with NaHCO3 (pH 8). Dissolved in standard cardioplegi c solution it was given every 30 minutes by coronary infusion at 20 de grees C during 3 hours of global ischemia. Glass electrode intramyocar dial pH, adenosine triphosphate (ATP) level, left ventricular contract ility (Dp/Dt) and compliance (-Dp/Dt), and other cardiovascular parame ters were measured frequently throughout ischemia and for 75 minutes t hereafter. In the buffer group (n = 6) myocardial pH remained above en try levels throughout the study period, adenosine triphosphate level r emained normal during ischemia, and Dp/Dt and -Dp/Dt at 75 minutes of reperfusion were above entry levels. In the NaHCO, group (n = 6) pH de clined and remained depressed throughout ischemia, adenosine triphosph ate level fell steadily and significantly throughout the experiment, a nd Dp/Dt and -Dp/Dt never regained entry levels. The difference in eac h parameter between the two groups was statistically significant (tt < 0.05). We conclude that control of myocardial acid-base equilibrium a lone during global ischemia will preserve myocardial function and mini mize reperfusion injury.