Arginine-vasopressin V1a receptor inhibition improves neurologic outcomes following an intracerebral hemorrhagic brain injury

Manaenko, Anatol; Fathali, Nancy; Khatibi, Nikan H.; Lekic, Tim; Hasegawa, Yu; Martin, Robert; Tang, Jiping; Zhang, Junyi

doi:10.1016/j.neuint.2011.01.018

Cited by 52 publications

(52 citation statements)

References 39 publications

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“…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] . So, AVP receptors may play an important role in the formation of edema after ICH through reduced BBB permeability or AQP4 levels, but the details of the mechanism are still unknown [52] . An in vivo microdialysis study shows that glutamate, taurine and asparagines accumulate transiently in extracellular fluids in the perihematoma region during the early period of ICH.…”

Section: Rbc Lysis Productionmentioning

confidence: 99%

“…Also, pretreated rats with PQQ significantly reduce the production of ROS after ICH, probably due to its antioxidant effects [96] . SR49059, an AVP V(1a) receptor competitive antagonist is proved to have a function of reducing brain edema and neurobehavioral deficits after ICH by decreasing the BBB disruption and AQP4 levels [51,52] . Animal experiments demonstrated that granulocyte-colony stimulating factor can protect ICH by reducing BBB permeation, cell apoptosis and brain edema [97] .…”

Section: Other Medicinesmentioning

confidence: 99%

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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%

Section: Other Medicinesmentioning

confidence: 99%

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

et al. 2016

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“…V1a antagonists have also been examined in animal models for the treatment of other disease states such as heart failure, cerebral vasospasm, brain edema, and gastric ulcers (294,322,549). Furthermore, in vitro studies have suggested a potential clinical application for V1a antagonists in treating cancer or renal disease (266,399,479).…”

Section: B V1a and V1b Receptor Antagonistsmentioning

confidence: 99%

“…It should be noted that a part of the intracranial artery causes vasodilatation upon AVP stimulation in an endothelium-dependent manner (264,386 Cerebral edema is a devastating consequence of brain injury that leads to compromised cerebral blood flow and worsening parenchymal damage. Blockade of the V1a receptor by SR49059 has been shown to significantly reduce intracranial pressure or cerebral edema after cortical contusion injury, intracerebral hemorrhage injury, or cerebral artery occlusion in animal models (275,322,384,457,487). Likewise, the V1a/V2 receptor antagonist YM087 (conivaptan) significantly reduced intracranial pressure and cerebral edema after traumatic brain injury (122,168).…”

Section: Cerebral Vasospasm and Brain Edemamentioning

confidence: 99%

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

323

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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“…A study investigating the inhibition of the arginine vasopressin (AVP) V1 receptor in mice after ICH, could thereby demonstrate a significant reduction in cerebral edema formation and significantly less neurobehavioral deficit in the mice treated with the competitive receptor antagonist [89]. They suggest AVP might be a key player of water homeostasis in the brain.…”

Section: Selection Of Most Interesting Candidatesmentioning

confidence: 99%

Potential Role of Blood Biomarkers in the Management of Nontraumatic Intracerebral Hemorrhage

Senn

Elkind

Montaner³

et al. 2014

Cerebrovasc Dis

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Background: Intracerebral hemorrhage (ICH), a subtype of stroke associated with high mortality and disability, accounts for 13% of all strokes. Basic and clinical research has contributed to our understanding of the complex pathophysiology of neuronal injury in ICH. Outcome rates, however, remain stable, and questions regarding acute management of ICH remain unanswered. Newer research is aiming at matching measured levels of serum proteins, enzymes, or cells to different stages of brain damage, suggesting that blood biomarkers may assist in acute diagnosis, therapeutic decisions, and prognostication. This paper provides an overview on the most promising blood biomarkers and their potential role in the diagnosis and management of spontaneous ICH. Summary: Information was collected from studies, reviews, and guidelines listed in PubMed up to November 2013 on blood biomarkers of nontraumatic ICH in humans.We describe the potential role and limitations of GFAP, S100B/RAGE, and ApoC-III as diagnostic biomarkers, F-Amyloid as a biomarker for etiological classification, and 27 biomarkers for prognosis of mortality and functional outcome. Within the group of prognostic markers we discuss markers involved in coagulation processes (e.g., D-Dimers), neuroendocrine markers (e.g., copeptin), systemic metabolic markers (e.g., blood glucose levels), markers of inflammation (e.g., IL-6), as well as growth factors (e.g., VEGF), and others (e.g., glutamate). Some of those blood biomarkers are agents of pathologic processes associated with hemorrhagic stroke but also other diseases, whereas others play more distinct pathophysiological roles and help in understanding the basic mechanisms of brain damage and/or recovery in ICH. Key Messages: Numerous blood biomarkers are associated with different pathophysiological pathways in ICH, and some of them promise to be useful in the management of ICH, eventually contributing additional information to current tools for diagnosis, therapy monitoring, risk stratification, or intervention. Up to date, however, no blood biomarker of ICH has been studied sufficiently to find its way into clinical routine yet; well-designed, large-scale, clinical studies addressing relevant clinical questions are needed. We suggest that the effectiveness of biomarker research in ICH might be improved by international cooperation and shared resources for large validation studies, such as provided by the consortium on stroke biomarker research (http://stroke-biomarkers.com/page.php?title=Resources). i 2014 S. Karger AG, Basel

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Arginine-vasopressin V1a receptor inhibition improves neurologic outcomes following an intracerebral hemorrhagic brain injury

Cited by 52 publications

References 39 publications

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Potential Role of Blood Biomarkers in the Management of Nontraumatic Intracerebral Hemorrhage

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