{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T10:21:19Z","timestamp":1762078879417},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,11,18]],"date-time":"2005-11-18T00:00:00Z","timestamp":1132272000000},"content-version":"vor","delay-in-days":5619,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Magnetic Resonance in Med"],"published-print":{"date-parts":[[1990,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Intracellular [Na<jats:sup>+<\/jats:sup>], [H<jats:sup>+<\/jats:sup>], and [ATP] and mechanical performance were measured in the isovolumic perfused rat heart during ischemia. The concentration of intracellular sodium, [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>, was determined by atomic absorption spectroscopy under control conditions, and [Na<jats:sup>+<\/jats:sup>] was monitored by <jats:sup>23<\/jats:sup>Na NMR spectroscopy at 1\u2010min intervals under control conditions and during global ischemia. [ATP], [H<jats:sup>+<\/jats:sup>], and [<jats:italic>P<\/jats:italic><jats:sub>i<\/jats:sub>] were measured by <jats:sup>31<\/jats:sup>PNMR in a separate group under identical conditions. The control [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub> measured by atomic absorption was 30.7 \u00b1 3.3 m<jats:italic>M<\/jats:italic>(mean \u00b1 SD, <jats:italic>n<\/jats:italic> = 6), and [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub> measured by NMR was 6.2 \u00b1 0.5 m<jats:italic>M<\/jats:italic>(<jats:italic>n<\/jats:italic> = 3). Brief ischemia (10 min) was associated with a 54% increase in [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub> which reversed completely with reperfusion. Developed pressure also returned to control values upon reperfusion. Prolonged ischemia (30 min) produced continuous further accumulation of sodium (0.53 m<jats:italic>M<\/jats:italic>\/min, <jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup> = 0.99). [H<jats:sup>+<\/jats:sup>] also increased approximately linearly early in ischemia (0.084 \u03bcM\/min, <jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup> = 0.97). The rate of increase in [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub> was more than 4000 times greater than the increase in [H<jats:sup>+<\/jats:sup>] on a molar basis. Nevertheless, [H<jats:sup>+<\/jats:sup>]\/[Na<jats:sup>+<\/jats:sup>] increased early in ischemia because the proportional change in [H<jats:sup>+<\/jats:sup>] was greater than that in [Na<jats:sup>+<\/jats:sup>] <jats:sub>i<\/jats:sub>. These results indicate that (1) intracellular sodium measured by NMR in the functioning heart is about 20% of total intracellular sodium; (2) intracellular acidosis and accumulation of sodium develop simultaneously during global ischemia; (3) increased intracellular sodium content is not in itself an indicator of irreversible injury; and (4) recovery of mechanical performance is associated with return of [Na<jats:sup>+<\/jats:sup>] (measured by NMR) to baseline after brief ischemia. The mechanism of the increase in sodium content detected by NMR is unknown. \u00a9 1990 Academic Press, Inc.<\/jats:p>","DOI":"10.1002\/mrm.1910150105","type":"journal-article","created":{"date-parts":[[2007,3,5]],"date-time":"2007-03-05T11:22:24Z","timestamp":1173093744000},"page":"33-44","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":93,"title":["Influence of global ischemia on intracellular sodium in the perfused rat heart"],"prefix":"10.1002","volume":"15","author":[{"given":"Craig R.","family":"Malloy","sequence":"first","affiliation":[]},{"given":"Douglas C.","family":"Buster","sequence":"additional","affiliation":[]},{"given":"M. C. A.","family":"Margarida Castro","sequence":"additional","affiliation":[]},{"given":"Carlos F. G. C.","family":"Geraldes","sequence":"additional","affiliation":[]},{"given":"F. Mark H.","family":"Jeffrey","sequence":"additional","affiliation":[]},{"given":"A. 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