Aquaporin-4 (AQP4) is the most abundant water channel in the brain,
and its inhibition before inducing focal ischemia, using the AQP4
inhibitor TGN-020, has been showed to reduce oedema in imaging studies.
水通道蛋白-4(AQP4)是大腦中最豐富的水通道,使用AQP4抑制劑誘導局灶性缺血後
被證明可以減少水腫。
所以抑制AQP4、AQP4不通會造成腦缺血,腦缺血自然就腦缺氧。
The primary aquaporins expressed in the mammalian brain are AQP1,
which is densely packed in choroid plexus cells lining the ventricles,
and AQP4, which is abundant in astrocytes and concentrated especially
in the end-feet structures that surround capillaries throughout
the brain and are present in glia limitans structures, notably
in osmosensory areas such the supraoptic nucleus.
在哺乳動物大腦中表達的主要水通道蛋白是AQP1,其密集地堆積在心室內的脈絡叢細胞中
,以及AQP4,其在星形膠質細胞中豐富並且尤其集中在圍繞整個腦的毛細血管的末端
- 腳結構中並且存在於 膠質細胞限制結構,特別是在諸如視上核之類的視覺區域。
錳增加AQP1的表達
錳(Mn)提升了水通道蛋白AQP-4(aquaporin-4)的膜表達
Paroxysmal sympathetic hyperactivity (sympathetic storm) in a patient
with permanent vegetative state.
具有永久植物狀態的患者陣發性交感神經過度活動(交感神經風暴)。
We report the first case of a patient in permanent vegetative state (PVS)
who developed paroxysmal sympathetic hyperactivity (sympathetic storm)
8 months after the hypoxic brain injury that lead to PVS.
我們報告了第一例患有永久性植物狀態(PVS)的患者,
該患者在導致PVS的缺氧性腦損傷後8個月出現陣發性交感神經過度活動(交感風暴)。
交感神經風暴 (sympathetic storming) 是由於腦部損傷後造成交感神經活化且
無法受副交感神經抑制所導致的臨床表現