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首页> 外文期刊>American Journal of Physiology >Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats.
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Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats.

机译：截瘫大鼠对心律失常的敏感性增加与Ca2 +调节蛋白的变化有关。

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摘要

Paraplegia may increase 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 that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ 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 (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(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca 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 abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (-28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.
机译：截瘫可能通过改变心脏的自主神经控制而增加对室性心律失常的敏感性。心脏自主控制的改变已被证明可以改变编码心脏Ca2 +调节蛋白的基因的表达。因此，我们检验了以下假设：截瘫会以增加对室性心律不齐的敏感性的方式改变Ca2 +调节蛋白的同时改变心脏电生理。为了验证这一假设，长期使用完整的（n = 10）和截瘫（n = 6）雄性Wistar大鼠测量房室（AV）间隔，窦周期长度，窦房结恢复时间（SNRT），经自发窦周期校正的SNRT （cSNRT），Wenckebach周期长度（WCL）以及诱发室性心律失常的电刺激阈值。此外，确定了完整（n = 8）和截瘫（n = 8）大鼠中肌膜（内膜）质网Ca2 + ATPase（SERCA），磷酸lamban和Na / Ca交换蛋白的相对蛋白丰度和mRNA表达。截瘫显着（P <0.05）减少了AV间隔（-25％），窦周期长度（-24％），SNRT（-28％），cSNRT（-53％），WCL（-19％）和电刺激诱发室性心律不齐的阈值（-48％）。截瘫显着增加了SERCA（45％）和Na / Ca交换子（40％）的相对蛋白丰度，并降低了磷lamban水平（-28％）。相反，截瘫大鼠仅Na / Ca交换子的相对mRNA表达增加（25％）。这些数据表明，截瘫以增强对室性心律不齐的敏感性的方式增强了心脏的电生理特性并改变了Ca2 +调节蛋白。

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