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Enhanced Sodium‐Calcium Exchange in the Infarcted Heart
Author(s) -
LITWIN SHELDON E.,
ZHANG DONGFANG
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04774.x
Subject(s) - calcium , sodium , chemistry , sodium calcium exchanger , cardiology , medicine , organic chemistry
A bstract : Arrhythmias and contractile dysfunction both contribute to the high morbidity and mortality in patients with congestive heart failure. Contractile dysfunction is generally believed to reflect a decrease in the amplitude of intracellular Ca 2+ transients, whereas tachyarrythmias are often initiated in the setting of cellular Ca 2+ overload. In a rabbit model of left ventricular dysfunction due to myocardial infarction, we found evidence that myocyte sarcoplasmic reticulum Ca 2+ content may be normal or even increased at slow stimulation rates. This may occur because prolonged action potential duration promotes Ca 2+ influx via the Na + /Ca 2+ exchanger. Despite preserved SR Ca 2+ content, intracellular Ca 2+ transients and contractions may be reduced in amplitude because of impaired synchronization of Ca 2+ release events throughout the myocyte.