Acute Vascular Disruption and Aquaporin 4 Loss After Stroke

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Acute vascular disruption and aquaporin 4 loss after stroke.

BACKGROUND AND PURPOSE Ischemic protection has been demonstrated by a decrease in stroke-infarct size in transgenic mice with deficient Aquaporin 4 (AQP4) expression. However, it is not known whether AQP4 is rapidly reduced during acute stroke in animals with normal AQP4 phenotype, which may provide a potential self-protective mechanism. METHODS Adult male rats underwent transient occlusion o...

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Aquaporin-4 gene disruption in mice protects against impaired retinal function and cell death after ischemia.

PURPOSE Water channel aquaporin (AQP)-4 is expressed in Muller cells in retina, which are similar to astroglial cells in the central nervous system, where AQP4 deletion protects against cytotoxic brain edema after cerebral ischemia. A transient ischemia-reperfusion model was used to determine whether AQP4 deletion in mice protects the retina. METHODS Retinal function and morphology were asses...

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Lack of sex-linked differences in cerebral edema and aquaporin-4 expression after experimental stroke.

Aquaporin-4 (AQP4) has been shown to be important in the evolution of stroke-associated cerebral edema. However, the role of AQP4 in stroke-associated cerebral edema as it pertains to sex has not been previously studied. The perivascular pool of AQP4 is important in the influx and efflux of water during focal cerebral ischemia. We used mice with targeted disruption of the gene encoding alpha-sy...

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Targets for vascular protection after acute ischemic stroke.

BACKGROUND Vascular damage caused by cerebral ischemia leads to edema, hemorrhage formation, and worsened outcomes in ischemic stroke patients. Therapeutic interventions need to be developed to provide vascular protection. The purpose of this review is to identify the pathophysiologic processes involved in vascular damage after ischemia, which may lead to strategies to provide vascular protecti...

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Weight Loss After Stroke

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ژورنال

عنوان ژورنال: Stroke

سال: 2009

ISSN: 0039-2499,1524-4628

DOI: 10.1161/strokeaha.108.523720