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1 Human Physiology, UC Davis, Davis, CA, USA
2 Anesthesiology, UC Davis, Davis, CA, USA
3 Surgery, UC Davis, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: seanderson{at}ucdavis.edu.
This study tests the hypothesis that in newborn hearts (as in adults) hypoxia and acidification stimulate increased Na uptake, in part via pH-regulatory Na/H exchange. Resulting increases in intracellular Na alter the force driving the Na/Ca exchanger and lead to increased intracellular Ca . NMR spectroscopy measured intracellular Na (Nai), Ca ([Ca]i), and pH (pHi) in isolated, Langendorff-perfused 4-7 day old rabbit hearts. After Na/K ATPase inhibition hypoxic hearts gained Na whereas normoxic controls did not (19±3.4 to 139±14.6 vs. 22±1.9 to 22±2.5 (SEM) mEq/kg dry wt, respectively). In normoxic hearts acidified using the NH4Cl prepulse, pHi fell rapidly and recovered while Nai rose from 31±18.2 to 117.7±20.5 mEq/kg dry wt. Both protocols caused increases in [Ca]i, however, [Ca]i increased less in newborn hearts than in adults (p < 0.05). Increases in Nai and [Ca]i were inhibited by the Na/H exchange inhibitor methylisobutylamiloride (MIA, 40µM - p < 0.05) as well as by increasing perfusate osmolarity (+30 mOsm) immediately prior to and during hypoxia (p < 0.05). The data support the hypothesis that in newborn hearts, like adults, increases in Nai and [Ca]i during hypoxia and after normoxic acidification are in large part the result of increased uptake via Na/H and Na/Ca exchange, respectively. However, for similar hypoxia and acidification protocols, this increase in [Ca]i is less in newborn than adult hearts.
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