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

The effects of respiratory and metabolic acidosis on myocardial contractility and energy production have been investigated in the perfused rat heart. Respiratory acidosis, produced by increasing the Pco2 , caused an 80% inhibition of pressure development at pH 6.7. When artificial buffers (plus HCI) 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. We conclude that both intracellular and extracellular H impair myocardial function but by separate mechanisms. Intracellular acidosis per se was shown to have 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 oxygen 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 data suggest that the fall of intracellular and extracellular pH were the principal determinants of the decline of pressure development in the tissue as a whole during the early stages of ischemia. We conclude that 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.