Enhanced sodium-calcium exchange in the infarcted heart: effects on sarcoplasmic reticulum content and cellular contractility.
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.
Litwin
Sheldon E
SE
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
Zhang
Dongfang
D
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*
D019831:Sodium-Calcium Exchanger; D012964:Sodium; D011188:Potassium