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β肾上腺素能阻断可预防癫痫持续状态后大鼠的心脏功能障碍。

β adrenergic blockade prevents cardiac dysfunction following status epilepticus in rats.

机构信息

Department of Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, UT 84112, United States.

出版信息

Epilepsy Res. 2012 May;99(3):233-9. doi: 10.1016/j.eplepsyres.2011.12.003. Epub 2011 Dec 29.

Abstract

Status epilepticus (SE) can result in temporary cardiac dysfunction in patients, characterized by reduced ejection fraction, decreased ventricular contractility, and alterations in electrical activity of the heart. Although reversible, the cardiac effects of seizures are acutely life threatening, and may contribute to the delayed mortality following SE. The precise mechanisms mediating acute cardiac dysfunctions are not known. These studies evaluated effects of self-sustaining limbic SE in rats on cardiac performance 24h following seizures, and determined if sympathetic nervous system activation during seizures contributed to cardiac dysfunction. Rats subjected to SE received either vehicle (saline) or the B1 adrenergic antagonist atenolol (AT) prior to and during 90 min of seizure activity. Control rats were similarly treated, except they did not undergo seizures. Twenty-four hours after SE, animals were anesthetized and catheterized for measurement of cardiac performance variables. Animals undergoing SE demonstrated significantly reduced cardiac output, decreased ventricular contractility and relaxation, increased blood pressure, and prolonged QT interval. However, heart rate was not altered. Treatment with AT prevented all changes in cardiac performance due to SE, and attenuated the increase in QT interval. These data demonstrate that SE in the rat results in cardiac dysfunction 24h following seizures, mediated by the sympathetic nervous system.

摘要

癫痫持续状态(SE)可导致患者出现暂时性心脏功能障碍,表现为射血分数降低、心室收缩力下降和心脏电活动改变。尽管这些心脏效应是可逆的,但癫痫发作时的心脏效应具有急性生命威胁,可能导致 SE 后延迟死亡。介导急性心脏功能障碍的确切机制尚不清楚。这些研究评估了在 SE 后 24 小时,大鼠自主维持的边缘性 SE 对心脏功能的影响,并确定癫痫发作期间交感神经系统的激活是否导致了心脏功能障碍。接受 SE 的大鼠在 SE 前和 90 分钟的发作期间接受了载体(生理盐水)或 B1 肾上腺素能拮抗剂阿替洛尔(AT)治疗。对照组大鼠也接受了类似的治疗,但没有进行癫痫发作。SE 后 24 小时,动物被麻醉并插入导管以测量心脏功能变量。进行 SE 的动物表现出明显的心输出量降低、心室收缩力和松弛性降低、血压升高和 QT 间期延长。然而,心率没有改变。AT 治疗可预防 SE 引起的所有心脏功能变化,并减轻 QT 间期的延长。这些数据表明,大鼠 SE 会导致 SE 后 24 小时的心脏功能障碍,这是由交感神经系统介导的。

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