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December 1, 1990AJP Cell Physiology180 citations

Na-H exchange in myocardium: effects of hypoxia and acidification on Na and Ca

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SASteven E. AndersonUniversity of California, DavisEMElizabeth MurphyCross-Cutting CardiologyCSCharles SteenbergenCross-Cutting Cardiology

Key Result

In Langendorff-perfused rabbit hearts, hypoxia increased intracellular Na content to 34.9 meq/kg dry wt compared to 13.6 meq/kg in normoxic controls.

Structured PICO

P
Population
Langendorff-perfused rabbit hearts subjected to hypoxia or acidification to evaluate intracellular Na and Ca dynamics.
I
Intervention
Hypoxia (with Na(+)-K(+)-ATPase inhibited by ouabain and/or K-free perfusion) or acidification (20 mM NH4Cl prepulse technique)
C
Comparator
Normoxic controls
O
Outcome
Intracellular Na content (Nai), Ca concentration ([Ca]i), pH (pHi), and high-energy phosphates measured by 23Na-, 19F-, and 31P-nuclear magnetic resonance (NMR)surrogate

Hypoxia-induced Na uptake in the myocardium appears to result from increased entry via Na-H exchange rather than decreased extrusion, leading to secondary Ca accumulation.

Main Result

Absolute Event Rate: 34.9% vs 13.6%

Abstract

Historically, increase in cell Na content during ischemic and hypoxic episodes were thought to result from impaired ATP production causing decreased Na(+)-K(+)-ATPase activity. Here we report the results of testing the alternate hypothesis that hypoxia-induced Na uptake is 1) the result of increased entry, as opposed to decreased extrusion 2) via Na-H exchange operating in a pH regulatory capacity and that cell Ca accumulation occurs via Na-Ca exchange secondary to collapse of the Na gradient. We used 23Na-, 19F-, and 31P-nuclear magnetic resonance (NMR) to measure intracellular Na content (Nai), Ca concentration ( Cai), pH (pHi), and high-energy phosphates in Langendorff-perfused rabbit hearts. When the Na(+)-K(+)-ATPase was inhibited by ouabain and/or K-free perfusion, hearts subjected to hypoxia gained Na at a rate greater than 10 times that of normoxic controls during the first 12.5 min Nai increased from 7.9 +/- 5.8 to 34.9 +/- 11.0 (SD) meq/kg dry wt compared with 11.1 +/- 16.3 to 13.6 +/- 9.0 meq/kg dry wt, respectively. When normoxic hearts were acidified using a 20 mM NH4Cl prepulse technique, pHi rapidly fell from 7.27 +/- 0.24 to 6.63 +/- 0.12 but returned to 7.07 +/- 0.10 within 20 min, while Na uptake was similar in rate and magnitude to that observed during hypoxia (24.5 +/- 13.4 to 132.1 +/- 17.7 meq/kg dry wt). During hypoxia and after NH4Cl washout, increases in Cai were similar in time course to those observed for Na.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cite This Study

Anderson et al. (1990) studied Myocardial hypoxia and acidification. Hypoxia vs. Normoxic controls was evaluated on Intracellular Na content (Nai) at 12.5 min. In Langendorff-perfused rabbit hearts, hypoxia increased intracellular Na content to 34.9 meq/kg dry wt compared to 13.6 meq/kg in normoxic controls.

synapsesocial.com/papers/6a63ecd1aab374d588f2ed40https://doi.org/10.1152/ajpcell.1990.259.6.c940
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