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1 Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: sdicarlo{at}med.wayne.edu.
Paraplegia may increase the susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes encoding cardiac calcium regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in calcium regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact (n = 10) and paraplegic (n = 6) male Wistar rats were chronically instrumented to measure atrioventricular interval (AV interval), sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach Cycle Length (WCL) and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endoplasmic) reticulum calcium ATPase (SERCA), phospholamban and sodium calcium exchanger were determined in intact (n = 8) and paraplegic (n = 8) rats. Paraplegia significantly (p < 0.05) reduced: AV interval (-25%), sinus cycle length (-24%), SNRT (-28%), cSNRT (-53%), WCL (-19%) and the electrical stimulation threshold to induce ventricular arrhythmia (-48%). Paraplegia significantly increased the relative protein abundance of SERCA (45%) and sodium calcium exchanger (40%) and decreased phospholamban (-28%). In contrast, only the relative mRNA expression of the sodium calcium exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters calcium regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias.
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