Metabolic acidosis induces a decrease in the developed force of cardiac muscle by affecting every step of the excitation--contraction coupling pathway. Due to transient worsening in intracellular
acidosis, the value of administering
sodium bicarbonate therapeutically during acute
acidosis has been questioned. An alternative therapeutic
drug,
Tris-hydroxymethyl aminomethane (THAM) has the advantage of diffusing into the intracellular space. This study was designed to evaluate the effects of
metabolic acidosis on myocardial performance and to determine the effects of alkalinization with
sodium bicarbonate, THAM, and their combination. Using a blood-perfused isolated heart preparation, left ventricular contractility and relaxation were measured at normal pH and during
metabolic acidosis (pH = 7.0).
Acidosis dramatically impaired myocardial contractility and relaxation. After buffering with
sodium bicarbonate, although plasma
bicarbonate concentration was normalized, pH remained below normal owing to an increased PaCO2. Contractility and relation were initially worsened, then slightly improved to return to control values. THAM uncompletely buffered
acidosis but significantly improved contractility and relaxation. The combination of THAM with
sodium bicarbonate perfectly buffered
acidosis without modifying PaCO2 and significantly improved contractility. The combination of THAM with
sodium bicarbonate is based on the ability of THAM to capture the CO2 produced by the
sodium bicarbonate buffer. This combination achieves a perfect correction of
metabolic acidosis and improves myocardial performance.