Carotid body stimulation as a potential intervention in sudden death in epilepsy.

Carotid body stimulation as a potential intervention in sudden death in epilepsy.
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DOI:
10.1016/j.yebeh.2022.108918
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发表时间:
2022-11
影响因子:
2.6
通讯作者:
Irazoqui, Pedro P.
Irazoqui, Pedro P.
中科院分区:
医学3区
文献类型:
--
作者:
Biggs, Ethan N.;Budde, Ryan B.;Jefferys, John G. R.;Irazoqui, Pedro P.

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探讨颈动脉体(CB)与癫痫猝死的相关机制。癫痫大鼠发作期激活储氧反射(OCRs)可导致致命性心肺衰竭,表现为类似于人类癫痫猝死(SUDEP)。CB与OCR通路密切相关;我们假设调节CB活性将深入了解这些死亡机制。Long-Evans大鼠用乌拉坦麻醉。记录包括:皮质电图、心电图、通过鼻热电偶的呼吸和血压(BP)。哺乳动物潜水反射(MDR)被通过鼻插管递送的冷水激活。反射和刺激试验重复多达16次(干预前4次,干预后12次)或直至死亡。在一些动物中,一个或两个颈动脉体失神经支配。在一些动物中,CB被电刺激,无论是否有MDR。用红藻氨酸(KA)诱导癫痫发作。没有癫痫发作和没有CB调制的动物在所有反射中存活。CB去神经的非癫痫动物在死亡前存活7.1 ± 5.4次反射,7只动物中只有1只存活超过12次试验阈值。无癫痫发作和无反射的CB电刺激引起显著的呼吸急促和低血压。有癫痫发作而无反射的CB电刺激需要更高的振幅来复制癫痫发作外所见的生理反应。无CB干预的癫痫动物存活3.2 ± 3.6次试验(每反射存活率42.0% ± 44.4%),7只动物中0只存活超过12次试验阈值。CB电刺激癫痫动物存活10.5 ± 4.7次发作试验(每反射存活率86.3% ± 35.0%),8只动物中有6只存活超过12次试验阈值。这些结果表明,在癫痫发作期间,CB刺激呼吸重新开始的能力受损。CB及其传入可能与人类致命性发作性呼吸暂停和SUDEP相关,CB刺激可能是这些死亡的相关干预技术。
To investigate carotid body (CB) mechanisms related to sudden death during seizure. Ictal activation of oxygen-conserving reflexes (OCRs) can trigger fatal cardiorespiratory collapse in seizing rats, which presents like human sudden unexpected death in epilepsy (SUDEP). The CB is strongly implicated in OCR pathways; we hypothesize that modulating CB activity will provide insight into these mechanisms of death. Long-Evans rats were anesthetized with urethane. Recordings included: electrocorticography, electrocardiography, respiration via nasal thermocouple, and blood pressure (BP). The mammalian diving reflex (MDR) was activated by cold water delivered through a nasal cannula. Reflex and stimulation trials were repeated up to 16 times (4 pre-intervention, 12 post-intervention) or until death. In some animals, one or both carotid bodies were denervated. In some animals, the CB was electrically stimulated, both with and without MDR. Seizures were induced with kainic acid (KA). Animals without seizure and with no CB modulation survived all reflexes. Non-seizing animals with CB denervation survived 7.1 ± 5.4 reflexes before death, and only 1 of 7 survived past the 12-trial threshold. Electrical CB stimulation without seizure and without reflex caused significant tachypnea and hypotension. Electrical CB stimulation with seizure and without reflex required higher amplitudes to replicate the physiological responses seen outside seizure. Seizing animals without CB intervention survived 3.2 ± 3.6 trials (per-reflex survival rate 42.0% ± 44.4%), and 0 of 7 survived past the 12-trial threshold. Seizing animals with electrical CB stimulation survived 10.5 ± 4.7 ictal trials (per-reflex survival rate 86.3% ± 35.0%), and 6 of 8 survived past the 12-trial threshold. These results suggest that, during seizure, the ability of the CB to stimulate a restart of respiration is impaired. The CB and its afferents may be relevant to fatal ictal apnea and SUDEP in humans, and CB stimulation may be a relevant intervention technique in these deaths.
DOI: 10.1016/j.eplepsyres.2018.10.003
发表时间: 2018-12
期刊: Epilepsy research
影响因子: 2.2
作者:
Budde RB;Arafat MA;Pederson DJ;Lovick TA;Jefferys JGR;Irazoqui PP
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DOI: 10.1113/jphysiol.1988.sp016988
发表时间: 1988-03-01
影响因子: 5.5
作者:
BUTLER, PJ;STEPHENSON, R
通讯作者: STEPHENSON, R
DOI: 10.1111/j.1528-1167.2011.03360.x
发表时间: 2012-02-01
期刊: EPILEPSIA
影响因子: 5.6
作者:
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DOI: 10.1113/jphysiol.2014.277574
发表时间: 2014-10-01
影响因子: 5.5
作者:
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发表时间: 2018-03-01
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