title: Vasopressin Hypersecretion-Associated Brain Edema Formation in Ischemic Stroke: Underlying Mechanisms.
abstract: BACKGROUND
  Brain edema formation is a major cause of brain damages and the high mortality of ischemic stroke. The aim of this review is to explore the relationship between ischemic brain edema formation and vasopressin (VP) hypersecretion in addition to the oxygen and glucose deprivation and the ensuing reperfusion injury.
  
  
  METHODS
  Pertinent studies involving ischemic stroke, brain edema formation, astrocytes, and VP were identified by a search of the PubMed and the Web of Science databases in January 2016. Based on clinical findings and reports of animal experiments using ischemic stroke models, this systematic review reanalyzes the implication of individual reports in the edema formation and then establishes the inherent links among them.
  
  
  RESULTS
  This systematic review reveals that cytotoxic edema and vasogenic brain edema in classical view are mainly under the influence of a continuous malfunction of astrocytic plasticity. Adaptive VP secretion can modulate membrane ion transport, water permeability, and blood-brain barrier integrity, which are largely via changing astrocytic plasticity. Maladaptive VP hypersecretion leads to disruptions of ion and water balance across cell membranes as well as the integrity of the blood-brain barrier. This review highlights our current understandings of the cellular mechanisms underlying ischemic brain edema formation and its association with VP hypersecretion.
  
  
  CONCLUSIONS
  VP hypersecretion promotes brain edema formation in ischemic stroke by disrupting hydromineral balance in the neurovascular unit; suppressing VP hypersecretion has the potential to alleviate ischemic brain edema.
authors.affiliation: Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
authors.forename: Shu-Wei
authors.initials: SW
authors.lastname: Jia
authors.affiliation: Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
authors.forename: Xiao-Yu
authors.initials: XY
authors.lastname: Liu
authors.affiliation: Department of Surgery, Albany Medical Center, Albany, New York.
authors.forename: Stephani C
authors.initials: SC
authors.lastname: Wang
authors.affiliation: Department of Physiology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China. Electronic address: yufengwang@ems.hrbmu.edu.cn.
authors.forename: Yu-Feng
authors.initials: YF
authors.lastname: Wang
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001929:Brain Edema / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D010641:Phenotype; D011379:Prognosis; D012307:Risk Factors; D015398:Signal Transduction; D020521:Stroke / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015854:Up-Regulation; D014667:Vasopressins / Q000378:metabolism*
chemical_list: D014667:Vasopressins
keywords: Aquaporin-4; astrocytes; brain edema formation; ischemic stroke; neuroendocrine; vasopressin