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Protection by benzamil against dysfunction and damage in rat myocardium after calcium depletion and repletion.

Abstract
Perfusion of the rat right ventricular wall muscle for 4 min with a Ca2(+)-free medium followed by perfusion with a Ca2(+)-containing solution resulted in a 42% recovery of developed tension, contracture, and a massive release of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) from the muscle. High concentrations (1-5 mM) of amiloride partially protected the ventricular wall from Ca2+ paradox-induced dysfunction. The inclusion of benzamil, an amiloride analogue, 2 min before and during the Ca2(+)-free perfusion period prevented contracture development, restored force development, and almost totally eliminated the release of CPK and LDH from the muscle. Contractile function was best protected by 10-50 microM benzamil. The results demonstrate the efficacy of benzamil as a protective agent against Ca2+ paradox-induced myocardial dysfunction and damage. In view of the known capacity of benzamil to block transsarcolemmal Na(+)-Ca2+ exchange, this study supports the involvement of elevated intracellular Na+ and a stimulation of Na(+)-Ca2+ exchange in this model of cardiac pathology.
AuthorsG N Pierce, T G Maddaford, E A Kroeger, E J Cragoe
JournalThe American journal of physiology (Am J Physiol) Vol. 258 Issue 1 Pt 2 Pg. H17-23 (Jan 1990) ISSN: 0002-9513 [Print] United States
PMID2301606 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • benzamil
  • Ouabain
  • Amiloride
  • Sodium
  • Calcium
Topics
  • Amiloride (analogs & derivatives, pharmacology)
  • Animals
  • Calcium (metabolism)
  • Heart Diseases (etiology, pathology, prevention & control)
  • Male
  • Myocardial Contraction (drug effects, physiology)
  • Myocardium (enzymology, metabolism)
  • Osmolar Concentration
  • Ouabain (pharmacology)
  • Rats
  • Rats, Inbred Strains
  • Sarcolemma (metabolism)
  • Sodium (metabolism)

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