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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Pt 1
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pubmed:dateCreated |
1991-1-31
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pubmed:abstractText |
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 [( Ca]i), 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 [Ca]i were similar in time course to those observed for Na.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/5-dimethylamiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Hydrogen Antiporter
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
259
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C940-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2175547-Amiloride,
pubmed-meshheading:2175547-Animals,
pubmed-meshheading:2175547-Anoxia,
pubmed-meshheading:2175547-Calcium,
pubmed-meshheading:2175547-Carrier Proteins,
pubmed-meshheading:2175547-Heart,
pubmed-meshheading:2175547-Hydrogen-Ion Concentration,
pubmed-meshheading:2175547-Kinetics,
pubmed-meshheading:2175547-Magnetic Resonance Spectroscopy,
pubmed-meshheading:2175547-Myocardium,
pubmed-meshheading:2175547-Rabbits,
pubmed-meshheading:2175547-Reference Values,
pubmed-meshheading:2175547-Sodium,
pubmed-meshheading:2175547-Sodium-Hydrogen Antiporter
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pubmed:year |
1990
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pubmed:articleTitle |
Na-H exchange in myocardium: effects of hypoxia and acidification on Na and Ca.
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pubmed:affiliation |
Department of Human Physiology, University of California, Davis 95616.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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