Innate Sleep Apnea in Spontaneously Hypertensive Rats Is Associated With Microvascular Rarefaction and Neuronal Loss in the preBötzinger Complex.
Innate Sleep Apnea in Spontaneously Hypertensive Rats Is Associated With Microvascular Rarefaction and Neuronal Loss in the preBötzinger Complex.
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作者：
睡眠呼吸暂停（SA）是对身体健康的主要威胁，并带来重大经济负担。它与合并症的相互作用以及引发合并症使得这些影响更加严重。睡眠呼吸暂停与高血压存在双向关系，这种关系会引发动脉粥样硬化/小动脉硬化，最终导致血管性痴呆。
为了更好地理解这些事件的后续影响，我们研究了成年自发性高血压大鼠的先天性睡眠呼吸暂停及其对认知的影响，这些大鼠存在一系列心血管疾病：我们使用体积描记法和脑电图/肌电图记录来评估睡眠 - 觉醒状态、呼吸参数以及睡眠呼吸紊乱；使用免疫细胞化学来评估血管和神经健康；分别使用强迫交替Y迷宫和巴恩斯迷宫来评估短期和长期记忆；并使用麻醉制剂来评估压力反射敏感性。
自发性高血压大鼠表现出更严重的睡眠呼吸紊乱，这是由于血管健康不佳导致前包钦格复合体神经元缺失所致。这些大鼠还表现出小血管白质病变，这是一种血管性痴呆，可能因睡眠呼吸暂停在海马体中引发的神经炎症而加剧，从而使短期和长期记忆的相关缺陷更加严重。
因此，我们推测高血压通过呼吸柱的血管损伤诱发睡眠呼吸暂停，最终导致吸气振荡器中的神经元缺失。这种睡眠呼吸暂停的诱发反过来又会独立地加剧高血压和神经炎症，增加血管性痴呆的发生率。
Sleep apnea (SA) is a major threat to physical health and carries a significant economic burden. These impacts are worsened by its interaction with, and induction of, its comorbidities. SA holds a bidirectional relationship with hypertension, which drives atherosclerosis/arteriolosclerosis, ultimately culminating in vascular dementia. To enable a better understanding of these sequelae of events, we investigated innate SA and its effects on cognition in adult-aged spontaneously hypertensive rats, which have a range of cardiovascular disorders: plethysmography and electroencephalographic/electromyographic recordings were used to assess sleep-wake state, breathing parameters, and sleep-disordered breathing; immunocytochemistry was used to assess vascular and neural health; the forced alteration Y maze and Barnes maze were used to assess short- and long-term memories, respectively; and an anesthetized preparation was used to assess baroreflex sensitivity. Spontaneously hypertensive rats displayed a higher degree of sleep-disordered breathing, which emanates from poor vascular health leading to a loss of preBötzinger Complex neurons. These rats also display small vessel white matter disease, a form of vascular dementia, which may be exacerbated by the SA-induced neuroinflammation in the hippocampus to worsen the related deficits in both long- and short-term memories. Therefore, we postulate that hypertension induces SA through vascular damage in the respiratory column, culminating in neuronal loss in the inspiratory oscillator. This induction of SA, which, in turn, will independently exacerbate hypertension and neural inflammation, increases the rate of vascular dementia.
影响因子：
4.7
作者：
Nanduri, Jayasri;Peng, Ying-Jie;Yuan, Guoxiang;Kumar, Ganesh K.;Prabhakar, Nanduri R.
通讯作者：
Prabhakar, Nanduri R.