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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/R1684    most recent 00219.2007v2 00219.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Horton, J. W. Articles by Maass, D. L. Search for Related Content PubMed PubMed Citation Articles by Horton, J. W. Articles by Maass, D. L.

ENVIRONMENTAL, EXERCISE AND RESPIRATORY PHYSIOLOGY

Burn injury decreases myocardial Na-K-ATPase activity: role of PKC inhibition

Jureta W. Horton, Jing Tan, D. Jean White, and David L. Maass

Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas

Submitted 30 March 2007 ; accepted in final form 16 July 2007

Cardiomyocyte sodium accumulation after burn injury precedes the development of myocardial contractile dysfunction. The present study examined the effects of burn injury on Na-K-ATPase activity in adult rat hearts after major burn injury and explored the hypothesis that burn-related changes in myocardial Na-K-ATPase activity are PKC dependent. A third-degree burn injury (or sham burn) was given over 40% total body surface area, and rats received lactated Ringer solution (4 ml·kg^–1·% burn^–1). Subgroups of rats were killed 2, 4, or 24 h after burn (n = 6 rats/time period), hearts were homogenized, and Na-K-ATPase activity was determined from ouabain-sensitive phosphate generation from ATP by cardiac sarcolemmal vesicles. Additional groups of rats were studied at several times after burn to determine the time course of myocyte sodium loading and the time course of myocardial dysfunction. Additional groups of sham burn-injured and burn-injured rats were given calphostin, an inhibitor of PKC, and Na-K-ATPase activity, cell Na⁺, and myocardial function were measured. Burn injury caused a progressive rise in cardiomyocyte Na⁺, and myocardial Na-K-ATPase activity progressively decreased after burn, while PKC activity progressively rose. Administration of calphostin to inhibit PKC activity prevented both the burn-related decrease in myocardial Na-K-ATPase and the rise in intracellular Na⁺ and improved postburn myocardial contractile performance. We conclude that burn-related inhibition of Na-K-ATPase likely contributes to the cardiomyocyte accumulation of intracellular Na⁺. Since intracellular Na⁺ is one determinant of electrical-mechanical recovery after insults such as burn injury, burn-related inhibition of Na-K-ATPase may be critical in postburn recovery of myocardial contractile function.

myocyte sodium; ventricular function; calphostin; protein kinase C inhibitor; rat burn injury model; protein kinase C activity