INTRACELLULAR PH DURING HYPOXIA IN NORMAL AND HYPERTROPHIED RIGHT VENTRICLE OF FERRET HEART

The effects of preventing oxidative phosphorylation on pH(i) were comp ared in papillary muscles from right ventricles of normal and pressure -overloaded ferret hearts, Hypertrophy was induced by pulmonary artery clipping for 30-45 days, pH(i) was recorded with pH-sensitive microel ectrodes. Resting pH(i) and the relationship between intracellular buf fering power and pH(i) were not modified by the hypertrophy. At 22 deg rees C, the initial intracellular alkalosis following exposure to oxyg en-free Tyrode solution (containing the reducing agent sodium dithioni te, 1 mM), as well as the transient acidosis on return to oxygenated s olution, were reduced in hypertrophied papillary muscles. During hypox ia, exposure to alpha-cyano-4-hydroxycinnamate (5 mh?) induced a large r intracellular acidification in hypertrophied than in control muscle. The initial alkalosis during hypoxia and the extra acidification on r ecovery from hypoxia were also significantly reduced in hypertrophied muscles at 35 degrees C, Moreover, the acidification during hypoxia wa s markedly accentuated in hypertrophied preparations at this temperatu re. [Mg2+](i) and [Ca2+](i) were also measured during metabolic inhibi tion, 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<0.0 01) and 1.3 (P<0.05) respectively. Upon application of 15 mM 2-deoxygl ucose, [Mg2+](i) was increased to a similar extent in control and hype rtrophied cells. It is concluded that right ventricular hypertrophy co uld modify creatine phosphate metabolism and the capacity to recruit a naerobic glycolysis.