Recovery of contractility and pHi during respiratory acidosis in ferret hearts: role of Na(+)-H+ exchange.

During acute respiratory acidosis, cardiac contractile pressure first drops but then recovers substantially. We investigated the mechanism of this response in isovolumic perfused ferret hearts. Developed pressure (DP) and its first derivative (dP/dt) were measured before, during, and after hypercapnia induced by equilibrating the perfusate with 15% CO2, rather than the 5% CO2 used in control. Intramyocardial pH (pHi) was measured by phosphorus nuclear magnetic resonance (NMR) spectroscopy. After the onset of hypercapnia (1-2 min), DP and +dP/dt reached minimal mean values of 37 +/- 2 and 39 +/- 3% of control, respectively. This early decline in myocardial contactility was followed by a partial recovery such that DP and +dP/dt had returned to 66 +/- 6 and 62 +/- 4% of control, respectively, by 14 min of hypercapnia. pHi fell from 7.17 +/- 0.01 in control to 6.88 +/- 0.11 after approximately 2 min of hypercapnia. Thereafter, pHi recovered linearly with a mean slope of 0.011 +/- 0.003 pH U/min. Ethylisopropylamiloride (10(-6) M), a blocker of Na(+)-H+ exchange, prevented the recovery of pHi during hypercapnia and attenuated the recovery of contractility by 40%. We conclude that the recovery of contractility during respiratory acidosis at least partially reflects an underlying recovery of pHi mediated by Na(+)-H+ exchange.