CORRECTION OF INTRAMYOCARDIAL HYPERCARBIC ACIDOSIS WITH SODIUM-BICARBONATE

Although it has been hypothesized that exogenously administered bicarb onate can exacerbate intramyocardial acidosis and compromise contracti le function, this phenomenon has not been demonstrated in an intact mo del in which intramyocardial pH (pH(int)), regional venous pCO(2), and regional contractile function have been simultaneously monitored. In 20 anesthetized dogs, we studied the effects of intracoronary infusion s of sodium bicarbonate NaHCO3 30 mEg over 15 min, on regional pH(int) , (glass electrode) and regional stroke work (SW, sonomicrometry) befo re and after creating systemic hypercarbic acidosis by hypoventilation . During NaHCO3 administration, regional coronary venous pCO(2) increa sed rapidly during the first minute (eucapnea; 34 +/- 7 to 55 +/- 18 m m Hg; hypercapnea: 70 +/- 15 to 98 +/- 23 mm Hg, P < 0.05 for both inc reases). Regional venous pH rose from 7.36 +/- .04 to 7.55 +/- .06 (P < 0.05) after the first minute of NaHCO3 infusion during eucapnea and from 7.09 +/- .09 to 7.22 +/- .09 (P < 0.05) during hypercapnea. Durin g the first minute of NaHCO3 infusion, pH(int) declined minimally. How ever, during the remaining 14 min of each infusion, pH(int) increased significantly (eucapnea: 7.19 +/- 0.10 to 7.43 +/- 0.12; hypercapnea: 6.86 +/- 0.14 to 7.02 +/- 0.15, P < 0.05 for both changes). Regional S W decreased significantly during the first minute of infusion, both du ring eucapnea (23,400 +/- 7,400 to 18,000 +/- 6,300 ergs/cm(2), P < 0. 05) and hypercapnea (27,000 +/- 9,100 to 25,000 +/- 10,000 ergs/cm(2), P < 0.05). The first minute of contractile dysfunction was followed b y recovery and ultimately supranormal contractile function during the remainder of each bicarbonate infusion. To test the hypothesis that tr ansient intracellular acidosis during bicarbonate infusions was undere stimated by measurements of pH(int), measurements of intracellular pH using the pH-sensitive dye, BCECF, were performed in isolated guinea p ig papillary muscles incubated in vitro. These measurements confirmed the presence of transient intracellular acidosis during bicarbonate in fusion. In conclusion, (1) the intracoronary administration of sodium bicarbonate causes a transient depression in myocardial contractile fu nction that is related to transient intracellular acidosis; and (2) de spite exacerbating hypercarbia, sodium bicarbonate ultimately neutrali zes intracellular acid and augments myocardial contractile function. ( C) 1994 Wiley-Liss, Inc.