Intracellular
acidosis may depress myocardial function and metabolism during
ischemia. In the present study, the function and metabolism of a globally ischemic, isovolumic cat left ventricle preparation, perfused with oxygenated Krebs-Ringer biocarbonate
solution, was examined. Addition of
tris(hydroxymethyl)-aminomethane (Tris) (15 mM) to the perfusate at physiologic pH and PCO2 increased performance during
ischemia to a greater extent and for a longer period than low PCO2 )15 mmHg), alkalotic (pH, 7.8) perfusate and a control
sucrose perfusate. Under nonischemic conditions the inotropic effect of Tris was only briefly greater than
sucrose perfusate. The inotropic effect of Tris during
ischemia did not appear to depend on changes in coronary flow, oxygen consumption,
sodium concentration, perfusate osmolality, or
catecholamine release. During
ischemia,
lactate production was unchanged with Tris, but increased with low PCO2-
alkalosis. Tissue levels of
ATP and
creatine phosphate for control ischemic hearts did not differ from Tris-perfused or low PCO2-
alkalosis hearts. Thus, Tris appears to exert an inotropic effect that is more prominent in ischemic than nonischemic myocardium. The results are consistent with the possibility that Tris acts as an intracellular
buffer to increase the efficiency of energy production and/or utilization during
ischemia.