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低通气在癫痫性猝死绵羊模型中的作用。

The role of hypoventilation in a sheep model of epileptic sudden death.

作者信息

Johnston S C, Horn J K, Valente J, Simon R P

机构信息

Department of Neurology, University of California, San Francisco, USA.

出版信息

Ann Neurol. 1995 Apr;37(4):531-7. doi: 10.1002/ana.410370416.

DOI:10.1002/ana.410370416
PMID:7717690
Abstract

Unexpected sudden death is a common event in otherwise healthy epileptics, though its etiology has remained unclear. Many authors have suggested cardiac arrhythmias as the cause, and limited data in humans and animal studies have supported this. However, autopsy series in humans have shown pulmonary edema, a phenomenon not compatible with a sudden arrhythmic death, as a possible cause. We developed a model of status epilepticus in unanesthetized, chronically instrumented sheep in which sudden death and pulmonary edema occur. Catecholamine levels and seizure type and duration did not differ between animals dying suddenly and those surviving. Benign arrhythmias were generated in all animals; in no case did an arrhythmia account for the death of an animal. Striking hypoventilation was demonstrated in the sudden death group but not in the surviving animals. Differences in peak left atrial and pulmonary artery pressures, and in extravascular lung water were also demonstrated; pulmonary edema did not account for the demise of the sudden death animals. Thus, our model of epileptic sudden death supports a role of central hypoventilation in the etiology of sudden unexpected death and confirms the association with pulmonary edema. The importance of arrhythmia in its pathogenesis is not confirmed.

摘要

意外猝死在其他方面健康的癫痫患者中是常见事件,但其病因仍不明确。许多作者认为心律失常是病因,人类和动物研究中的有限数据支持了这一点。然而,人类尸检系列显示肺水肿作为可能病因,这是一种与心律失常性猝死不相符的现象。我们在未麻醉、长期植入仪器的绵羊中建立了癫痫持续状态模型,其中会发生猝死和肺水肿。突然死亡的动物和存活动物之间的儿茶酚胺水平、癫痫发作类型和持续时间没有差异。所有动物都出现了良性心律失常;没有一例心律失常导致动物死亡。在猝死组中显示出明显的通气不足,而存活动物中未出现。左心房和肺动脉峰值压力以及血管外肺水也存在差异;肺水肿并不能解释猝死动物的死亡。因此,我们的癫痫性猝死模型支持中枢性通气不足在意外猝死病因中的作用,并证实了与肺水肿的关联。心律失常在其发病机制中的重要性未得到证实。

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