Effects of acidosis and ischemia on contractility and intracellular pH of rat heart.

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Abstract
The effects of respiratory and metabolic acidosis on myocardial contractility and energy production were investigated in the perfused rat heart. Respiratory acidosis, produced by increasing the PCO2 [partial CO2 pressure], caused an 80% inhibition of pressure development at pH 6.7. When artificial buffers (plus HCl) were used in place of bicarbonate and CO2, only a 30% inhibition of pressure development was observed at pH 6.7. Respiratory acidosis produced a greater intracellular acidosis than artificial buffer acidosis at the same extracellular pH. Both intracellular and extracellular H+ impair myocardial function but by separate mechanisms. Intracellular acidosis per se had little effect on the balance between energy production and energy utilization, and energy stores were relatively well maintained under these conditions. The contribution of intracellular acidosis to ischemic heart failure was examined using an ischemia model in which the coronary flow was decreased during diastole. Consequent restricted O2 delivery produced a pattern of heterogeneous oxygenation. A fall in effluent pH was concomitant with the decline in myocardial performance, and the intracellular pH fell as the extracellular space became more acidotic. The fall of intracellular and extracellular pH was the principal determinant of the decline of pressure development in the tissue as a whole during the early stages of ischemia. Mechanical function is depressed in ischemia not only in anoxic regions of the heart, but also in adjacent aerobic regions because of the pH change.