INTRACELLULAR BUFFERING OF HEART AND SKELETAL-MUSCLES DURING ONSET OF HYPERCAPNIA

Changes in the total CO2 content of tissues were determined in order to characterize variations in intracellular acid-base parameters during the onset of hypercapnia. Within 2 min after an increment in the CO2 tension of the inspired air of rats, there were large increases in the intracellular bicarbonate concentrations of both cardiac and skeletal muscles. Greater changes occurred in the heart, and its intracellular pH remained near normal during the 1st h of hypercapnia, but there was an intracellular acidosis in skeletal muscle. This greater capacity of the heart of buffer excess CO2 was linked to an increased movement of bicarbonate ions into and/or hydrogen ions out of cardiac cells during hypercapnia. Yet, the buffer capacity of the heart was not compromised by metabolic acidosis during which there was a greatly reduced extracellular bicarbonate ion concentration and a greatly increased extracellular H+ concentration. The intracellular pH of the cardiac ventricle was stable following the imposition of a noncarbonic acid load on normocapnic rats.