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Ann Thorac Surg 1994;57:1590-1595
© 1994 The Society of Thoracic Surgeons

Articles

Aminosulfonic acid buffer preserves myocardium during prolonged ischemia

Henry Swan, MD*, Michael Cowan, MB, Michael Tornabene, CCP, Lewis Owens, MD

Institute for Biological Research, Department of Surgery, University of Colorado School of Medicine, Denver, Colorado, USA

Accepted for publication October 26, 1993.

* Address reprint requests to Dr Swan, 6700 W Lakeridge Rd, Lakewood, CO 80227.

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 °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 myocaidial function and minimize reperfusion injury.






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