|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
|
|
|
|||||||||
|
|||||||||||
|
J Am Coll Cardiol, 1998; 31:701-706 © 1998 by the American College of Cardiology Foundation |
Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA. MCPH@AOL.com
OBJECTIVES: We sought to determine whether heart failure results in loss of cardiac magnesium sufficient to alter cellular electrophysiology. BACKGROUND: Free magnesium has numerous intracellular roles affecting metabolism, excitability and RNA synthesis. Total cardiac magnesium content is reduced in heart failure, but it is unclear whether magnesium loss is primary or iatrogenic. Furthermore, it is unknown whether free magnesium levels are affected or whether a change in free magnesium would alter cellular electrophysiology. METHODS: Eight mongrel dogs underwent demand ventricular pacing (VVI) at 250 beats/min for 3 weeks to induce heart failure. Sublingual epithelial magnesium was measured before pacing and at death. Left ventricular myocytes were isolated and loaded with Mag-Indo-1 to measure free magnesium ([Mg2+]i); myocytes from eight normal dogs served as controls. To test whether changes in [Mg2+]i in this range could alter cellular repolarization, current-clamped myocytes were dialyzed with 0.5 or 1.0 mmol/liter MgCl2. RESULTS: Mean sublingual epithelial magnesium fell significantly in the paced animals, from 36.9 +/- 0.5 to 33.9 +/- 0.7 mEq/liter (p < 0.01). Mean cardiac [Mg2+]i was significantly lower in the dogs with heart failure--0.49 +/- 0.06 versus 1.06 +/- 0.15 mmol/liter (p < 0.003). Time to 90% repolarization was significantly shorter in cells dialyzed with 1.0 mmol/liter compared with 0.5 mmol/liter MgCl2 in myocytes from normal dogs or dogs with heart failure (596 +/- 34 vs. 760 +/- 58 ms in normal dogs and 586 +/- 29 vs. 838 +/- 98 ms in dogs with heart failure; p < 0.05 for each). CONCLUSIONS: Experimental heart failure results in both tissue and cardiac magnesium loss in the absence of drug therapy. Free cardiac magnesium is significantly reduced, possibly contributing to abnormal repolarization in heart failure.
This article has been cited by other articles:
|
|
 |
|
  A. Sridhar, S. J. Dech, V. A. Lacombe, T. S. Elton, S. A. McCune, R. A. Altschuld, and C. A. Carnes Abnormal diastolic currents in ventricular myocytes from spontaneous hypertensive heart failure rats Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2192 - H2198. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Duke, P. M. Hopkins, P. J. Halsall, and D. S. Steele Mg2+ dependence of Ca2+ release from the sarcoplasmic reticulum induced by sevoflurane or halothane in skeletal muscle from humans susceptible to malignant hyperthermia Br. J. Anaesth., September 1, 2006; 97(3): 320 - 328. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Hinterseer, M. Irlbeck, L. Ney, B.-M. Beckmann, A. Pfeufer, G. Steinbeck, and S. Kaab Acute respiratory distress syndrome with transiently impaired left ventricular function and Torsades de Pointes arrhythmia unmasking congenital long QT syndrome in a 25-yr-old woman Br. J. Anaesth., August 1, 2006; 97(2): 150 - 153. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Brunet, T. Scheuer, R. Klevit, and W. A. Catterall Modulation of CaV1.2 Channels by Mg2+ Acting at an EF-hand Motif in the COOH-terminal Domain J. Gen. Physiol., September 26, 2005; 126(4): 311 - 323. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. B. Silver Development of Cellular Magnesium Nano-Analysis in Treatment of Clinical Magnesium Deficiency J. Am. Coll. Nutr., December 1, 2004; 23(6): 732S - 737S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. McCurley, S. U. Hanlon, S.-k. Wei, E. F. Wedam, M. Michalski, and M. C. Haigney Furosemide and the progression of left ventricular dysfunction in experimental heart failure J. Am. Coll. Cardiol., September 15, 2004; 44(6): 1301 - 1307. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. M. van den Bergh, A. Algra, and G. J.E. Rinkel Electrocardiographic Abnormalities and Serum Magnesium in Patients With Subarachnoid Hemorrhage Stroke, March 1, 2004; 35(3): 644 - 648. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-k. Wei, A. Ruknudin, S. U. Hanlon, J. M. McCurley, D. H. Schulze, and M. C.P. Haigney Protein Kinase A Hyperphosphorylation Increases Basal Current but Decreases {beta}-Adrenergic Responsiveness of the Sarcolemmal Na+-Ca2+ Exchanger in Failing Pig Myocytes Circ. Res., May 2, 2003; 92(8): 897 - 903. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Kiyosue Removal of intracellular Mg2+ activates cardiac Na+/Ca2+ exchanger Cardiovasc Res, February 1, 2002; 53(2): 290 - 291. [Full Text] [PDF]
|
|
|
|
|
|
S.-k. Wei, J. F Quigley, S. U Hanlon, B. O'Rourke, and M. C.P Haigney Cytosolic free magnesium modulates Na/Ca exchange currents in pig myocytes Cardiovasc Res, February 1, 2002; 53(2): 334 - 340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. J Griffiths Calcium handling and cell contraction in rat cardiomyocytes depleted of intracellular magnesium Cardiovasc Res, July 1, 2000; 47(1): 116 - 123. [Abstract] [Full Text] [PDF]
|
|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
