Effect of arginine vasopressin on the cortex edema in the ischemic stroke of Mongolian gerbils

Zhao, Xueyan; Wu, Chunfang; Yang, Jun; Gao, Yang; Sun, Fang-Jie; Wang, Daxin; Wang, Changhong; Lin, Bei

doi:10.1016/j.npep.2015.01.003

Cited by 17 publications

(7 citation statements)

References 41 publications

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“…Experiments showed that AVP can induce the formation of brain edema by effects on astrocytes after ischemic stroke and the induction can be decreased by AVP receptors antagonist [49,50] . And, animal tests have found that AVP receptors antagonist SR49059 significantly decreases cerebral edema at 24 and 72 h post-ICH injury and improved neurobehavioral deficits at 72 h [51] .…”

Section: Rbc Lysis Productionmentioning

confidence: 99%

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

et al. 2016

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Background: Intracerebral hemorrhage (ICH) is a subtype of stroke with a severe high mortality and disability rate and accounts for about 10-15% of all strokes. The oppression and destruction by hematoma to brain tissue cause the primary brain injury. The inflammation and coagulation response after ICH would accelerate the formation of brain edema around hematoma, resulting in a more severe and durable injury. Currently, treatments for ICH are focusing on the primary injury including reducing intracranial hypertension, blood pressure control, and rehabilitation. There is a short-of-effective medical treatment for secondary inflammation and reducing brain edema in ICH patients. So, it is very important to study on the relationship between brain edema and ICH. Summary: Many molecular and cellular mechanisms contribute to the formation and progress of brain edema after ICH; inhibition of brain edema provides favorable outcome of ICH. Key Messages: This review mainly discusses the pathology and mechanism of brain edema, the effects of brain edema on ICH, and the methods of treating brain edema after ICH.

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Section: Rbc Lysis Productionmentioning

confidence: 99%

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

et al. 2016

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“…On the other hand, AVP affects astrocytic functions and regulates the onset of ischemic stroke [ 28 ]. For example, AVP induces ischemia-evoked brain edema in the setting of ischemic stroke [ 26 ]. Moreover, AVP induces production of inflammatory molecules after cerebral edema [ 24 ], and it subsequently enhances disruption of the BBB [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…Arginine-vasopressin (AVP) induces production of inflammatory molecules after cerebral edema [ 24 ], and it is associated with disruption of the blood-brain barrier (BBB) [ 25 ]. In addition, AVP enhances ischemia-evoked edema in the cortex in ischemic strokes [ 26 ]. It was further demonstrated that the AVP V1 receptor inhibitor reduced ischemia-induced cerebral edema following stroke [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Arginine vasopressin altered the expression of monocarboxylate transporters in cultured astrocytes isolated from stroke-prone spontaneously hypertensive rats and congenic SHRpch1_18 rats

Yamagata

Takahashi

Akita

et al. 2017

J Neuroinflammation

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BackgroundAstrocytes support a range of brain functions as well as neuronal survival, but their detailed relationship with stroke-related edema is not well understood. We previously demonstrated that the release of lactate from astrocytes isolated from stroke-prone spontaneously hypertensive rats (SHRSP/Izm) was attenuated under stroke conditions. The supply of lactate to neurons is regulated by astrocytic monocarboxylate transporters (MCTs). The purpose of this study was to examine the contributions of arginine vasopressin (AVP) and/or hypoxia and reoxygenation (H/R) to the regulation of MCTs and neurotrophic factor in astrocytes obtained from SHRSP/Izm and congenic SHRpch1_18 rats.MethodsWe compared AVP-induced lactate levels, MCTs, and brain-derived neurotrophic factor (BDNF) in astrocytes isolated from SHRSP/Izm, SHRpch1_18, and Wistar Kyoto rats (WKY/Izm). The expression levels of genes and proteins were determined by PCR and Western blotting (WB).ResultsThe production of lactate induced by AVP was increased in astrocytes from all three strains. However, the levels of lactate were lower in SHRSP/Izm and SHRpch1_18 animals compared with the WKY/Izm strain. Gene expression levels of Slc16a1, Slc16a4, and Bdnf were lowered by AVP in SHRSP/Izm and SHRpch1_18 rats compared with WKY/Izm. The increase of MCT4 that was induced by AVP was blocked by the addition of a specific nitric oxide (NO) chelator, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO). Furthermore, AVP increased the expression of iNOS and eNOS proteins in WKY/Izm and SHRSP/Izm rat astrocytes. However, the iNOS expression levels in SHRSP astrocytes differed from those of WKY/Izm astrocytes. The increase of MCT4 protein expression during AVP treatment was blocked by the addition of a specific NF-kB inhibitor, pyrrolidine dithiocarbamate (PDTC). The induction of MCT4 by AVP may be regulated by NO through NF-kB.ConclusionsThese results suggest that the expression of MCTs mediated by AVP may be regulated by NO. The data suggest that AVP attenuated the expression of MCTs in SHRSP/Izm and SHRpch1_18 astrocytes. Reduced expression of MCTs may be associated with decreased lactate production in SHRSP.

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“…AVP induced the cell proliferation and collagen production of cardiac fibroblasts (Xie et al, 2013). AVP antagonists could also attenuate brain damage (Marmarou et al, 2014;Zhao et al, 2015).…”

Section: Introductionmentioning

confidence: 99%