title: An increase in intracellular [Na+] during Ca2+ depletion is not related to Ca2+ paradox damage in rat hearts.
abstract: Ca2+ paradox damage has been suggested to be determined by Na+ entry during Ca2+ depletion and exchange of Na+ for Ca2+ during Ca2+ repletion. With the use of 23Na nuclear magnetic resonance, we previously observed a Ca2+ paradox without a prior Na+ increase. We have now demonstrated a Na+ increase during Ca2+ and Mg2+ depletion without the occurrence of the Ca2+ paradox during Ca2+ repletion. Isolated rat hearts were perfused for 20 min with a Ca(2+)-free or a Ca(2+)- and Mg(2+)-free (Ca2+/Mg(2+)-free) solution under hypothermic conditions (20 and 25 degrees C). Intracellular Na+ concentration ([Na+]i) increased from 11.9 +/- 1.2 to 26.9 +/- 5.8 mM (P < 0.001) during Ca2+/Mg(2+)-free perfusion at 20 degrees C, whereas no significant change in [Na+]i occurred during 20 min of Ca(2+)-free perfusion at 20 degrees C. In addition, we confirmed that [Na+]i did not change significantly during 20 min of normothermic Ca(2+)-free perfusion. Creatine kinase release during normothermic Ca2+ repletion in the 20 degrees C groups was approximately 10% and in the 25 degrees C groups 75% of the release in the normothermia group. Recovery of rate-pressure product was approximately 50% in the 20 degrees C groups versus 0% in the normothermia group. In conclusion, hypothermic Ca2+/Mg(2+)-free perfusion results in a significant increase of [Na+]i, which does not contribute to the extent of the Ca2+ paradox on normothermic Ca2+ repletion.
authors.affiliation: Department of Cardiology, University Hospital, Utrecht, The Netherlands.
authors.forename: M A
authors.initials: MA
authors.lastname: Jansen
authors.forename: C J
authors.initials: CJ
authors.lastname: Van Echteld
authors.forename: T J
authors.initials: TJ
authors.lastname: Ruigrok
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D003080:Cold Temperature; D003402:Creatine Kinase / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D019906:Nuclear Magnetic Resonance, Biomolecular; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000503:physiopathology; D012964:Sodium / Q000502:physiology*
chemical_list: D012964:Sodium; D003402:Creatine Kinase; D002118:Calcium