Intracellular pH during hypoxia in normal and hypertrophied right ventricle of ferret heart.

The effects of preventing oxidative phosphorylation on pHi were compared in papillary muscles from right ventricles of normal and pressure-overloaded ferret hearts. Hypertrophy was induced by pulmonary artery clipping for 30-45 days. pHi was recorded with pH-sensitive microelectrodes. Resting pHi and the relationship between intracellular buffering power and pHi were not modified by the hypertrophy. At 22 degrees C, the initial intracellular alkalosis following exposure to oxygen-free Tyrode solution (containing the reducing agent sodium dithionite, 1 mM), as well as the transient acidosis on return to oxygenated solution, were reduced in hypertrophied papillary muscles. During hypoxia, exposure to alpha-cyano-4-hydroxycinnamate (5 mM) induced a larger intracellular acidification in hypertrophied than in control muscle. The initial alkalosis during hypoxia and the extra acidification on recovery from hypoxia were also significantly reduced in hypertrophied muscles at 35 degrees C. Moreover, the acidification during hypoxia was markedly accentuated in hypertrophied preparations at this temperature. [Mg2+]i and [Ca2+]i were also measured during metabolic inhibition, using mag-fura-2 and fura-2 respectively, in isolated cells from control and hypertrophied right ventricles. Hypertrophy increased the resting level of [Ca2+]i and of [Mg2+]i by a factor of 2.5 (P < 0.001) and 1.3 (P < 0.05) respectively. Upon application of 15 mM 2-deoxyglucose, [Mg2+]i was increased to a similar extent in control and hypertrophied cells. It is concluded that right ventricular hypertrophy could modify creatine phosphate metabolism and the capacity to recruit anaerobic glycolysis.