INTRACELLULAR PH AND INTRINSIC H+ BUFFERING CAPACITY IN NORMAL AND HYPERTROPHIED RIGHT VENTRICLE OF FERRET HEART

Objective: To answer the questions: (a) What is the effect of hypertro phy on the intracellular pH (pH(i)) and buffering power of cardiac mus cle, and (b) How does hypertrophy affect the ability of cardiac muscle to recover from intracellular acidosis induced by hypoxia. Methods: I n nominally HCO3--free, HEPES-buffered Tyrode solution (35 degrees C), pH(i) and the intrinsic buffering power(beta(i), measured in the pres ence of amiloride) was investigated using pH-sensitive microelectrodes . Results: beta(i) was similar in both preparations (25 mM/pH unit at pH(i) 7.04). beta(i) was inversely related to pH(i) but the relationsh ip was not significantly modified by hypertrophy. In the absence of am iloride, the time constant of pH(i) recovery (tau(r)) on removal of NH 4+, was similar in normal (4.0 +/- 0.2 min, n = 5) and in hypertrophie d muscles (4.3 +/- 0.3 min, n = 4; n.s.). In both preparations, net ac id extrusion (J(H)) was similarly increased at lower values of pH(i). Lowering temperature from 35 degrees to 22 degrees caused an alkaliniz ation (0.15 pH units) of pH(i). At 22 degrees C the mean values of pH( i), beta(i), tau(r) and J(H) were similar in normal and in hypertrophi ed muscles. At both temperatures and in both groups of preparations, r ecovery of pH(i) following hypoxia is approximately exponential. The t ime constant of recovery of pH(i) following hypoxia (tau(m)) at 22 deg rees C was not significantly different in hypertrophied muscles (7.2 /- 0.9 min, n = 8) compared to controls (10.6 +/- 1.8 min, n = 13). Ho wever, at 35 degrees C, there was a significant difference in the mean values of tau(rh) which was smaller for hypertrophied muscles (3.9 +/ - 0.3 min, n = 7) than for normal (7.1 +/- 1.1 min, n = 4, P < 0.005). For pH(i) 6.8-7.0, net acid extrusion in hypertrophied preparations w as increased by a factor of 4 compared to normal. Conclusions: The int racellular buffering capacity and the pH(i) regulating capacity via Na +/H+ exchange are not significantly modified by right ventricular hype rtrophy in ferret heart. The faster pH(i) recovery from hypoxia-induce d acidification can be interpreted in terms of the role of lactate eff lux in pH(i) control. The possible role of energy compartmentalization , its influence on the Na+ gradient and thus on pH(i) control after hy poxia, is discussed.