title: Enhanced sodium-calcium exchange in the infarcted heart: effects on sarcoplasmic reticulum content and cellular contractility.
abstract: 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.
authors.affiliation: Division of Cardiology, Salt Lake City Veterans Affairs Medical Center and the University of Utah, Salt Lake City, Utah 84148, USA. sheldon.litwin@hsc.utah.edu
authors.forename: Sheldon E
authors.initials: SE
authors.lastname: Litwin
authors.forename: Dongfang
authors.initials: D
authors.lastname: Zhang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D032342:Muscle Cells / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D009203:Myocardial Infarction / Q000503:physiopathology*; D011188:Potassium / Q000378:metabolism*; D011817:Rabbits; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger / Q000502:physiology*
chemical_list: D019831:Sodium-Calcium Exchanger; D012964:Sodium; D011188:Potassium