The Annals of Thoracic Surgery, Vol 57, 1590-1595, Copyright © 1994 by The Society of Thoracic Surgeons
Aminosulfonic acid buffer preserves myocardium during prolonged ischemia
H Swan, M Cowan, M Tornabene and L Owens
Department of Surgery, University of Colorado School of Medicine, Denver.
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 acid
buffer composition, 3:1 molar equivalents NaMOPS to HEPES, 0.2 mol/L, was
compared with NaHCO3 (pH 8). Dissolved in standard cardioplegic solution it
was given every 30 minutes by coronary infusion at 20 degrees C during 3
hours of global ischemia. Glass electrode intramyocardial pH, adenosine
triphosphate (ATP) level, left ventricular contractility (Dp/Dt) and
compliance (-Dp/Dt), and other cardiovascular parameters were measured
frequently throughout ischemia and for 75 minutes thereafter. In the buffer
group (n = 6) myocardial pH remained above entry levels throughout the
study period, adenosine triphosphate level remained normal during ischemia,
and Dp/Dt and - Dp/Dt at 75 minutes of reperfusion were above entry levels.
In the NaHCO3 group (n = 6) pH declined and remained depressed throughout
ischemia, adenosine triphosphate level fell steadily and significantly
throughout the experiment, and Dp/Dt and -Dp/Dt never regained entry
levels. The difference in each parameter between the two groups was
statistically significant (p < 0.05). We conclude that control of
myocardial acid-base equilibrium alone during global ischemia will preserve
myocardial function and minimize reperfusion injury.
