Role of Nitric Oxide in Blood-Brain Barrier Permeability, Brain Edema and Cell Damage Following Hyperthermic Brain Injury. An Experimental Study Using EGB-761 and Gingkolide B Pretreatment in the Rat

Sharma, Hari Shanker; Drieu, Katy; Alm, P.; Westman, Jan

doi:10.1007/978-3-7091-6346-7_17

Cited by 50 publications

(42 citation statements)

References 14 publications

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“…61,62 Other proteins that are up-regulated, and whose function results in degradation of the blood-brain barrier, include nitric oxide synthase (NOS), either inducible NOS 63 or neuronal NOS. 64 Notably, these various molecular mechanisms establish the important concept that constitutively expressed participants may play only a limited part, and up-regulation of a family of proteins that change the permeability of the blood-brain barrier may well be the norm.…”

Section: Permeability Poresmentioning

confidence: 99%

Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications

Simard

Kent

Chen

et al. 2007

The Lancet Neurology

686

619

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Focal cerebral ischaemia and post-ischaemic reperfusion cause cerebral capillary dysfunction, resulting in oedema formation and haemorrhagic conversion. There are substantial gaps in understanding the pathophysiology, especially regarding early molecular participants. Here, we review physiological and molecular mechanisms involved. We reaffirm the central role of Starling's principle, which states that oedema formation is determined by the driving force and the capillary "permeability pore". We emphasise that the movement of fluids is largely driven without new expenditure of energy by the ischaemic brain. We organise the progressive changes in osmotic and hydrostatic conductivity of abnormal capillaries into three phases: formation of ionic oedema, formation of vasogenic oedema, and catastrophic failure with haemorrhagic conversion. We suggest a new theory suggesting that ischaemia-induced capillary dysfunction can be attributed to de novo synthesis of a specific ensemble of proteins that determine osmotic and hydraulic conductivity in Starling's equation, and whose expression is driven by a distinct transcriptional program.Correspondence to: Dr J Marc Simard, Department of Neurosurgery, 22 S. Greene St., Suite 12SD, Baltimore, MD 21201−1595, USA msimard@smail.umaryland.edu. Contributors JMS originated the overall concept for this review and wrote the first and second drafts. TAK contributed to and helped edit the first and second drafts, and supplied important citations. MC participated in the original work on the sections on the NC Ca-ATP channel and contributed to the first draft. KVT did the computer analysis of the gene promoter regions. VG engaged in numerous intellectual exchanges with JMS during formulation of concepts for this review.Conflict of interest JMS and MC have applied for a US patent, "A novel non-selective cation channel in neural cells and methods for treating brain swelling" (application number 10/391,561). NIH Public Access

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Section: Permeability Poresmentioning

confidence: 99%

Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications

Simard

Kent

Chen

et al. 2007

The Lancet Neurology

686

619

View full text Add to dashboard Cite

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“…The excessive production of NO, however, is considered to be detrimental to CNS under pathological conditions (21,22). Over the past decade and a half, S-nitrosothiols (i.e.…”

mentioning

confidence: 99%

S-Nitrosoglutathione Induces Ciliary Neurotrophic Factor Expression in Astrocytes, Which Has Implications to Protect the Central Nervous System under Pathological Conditions

Paintlia

Singh

et al. 2013

Journal of Biological Chemistry

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Background: CNTF plays an important role in brain development and injury. Results: S-Nitrosoglutathione induces CNTF expression in astrocytes via NO signaling dependent PPAR-␥ transactivation. Conclusion: NO signaling in astrocytes favors the beneficial outcomes of reactive astrogliosis. Significance: Endogenously produced NO or its exogenous source has potential to modulate the outcomes of reactive astrogliosis in vivo.

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“…Environmental hyperthermia decreases endogenous antioxidants and increases nitric oxide (NO), superoxide production, and consequent lipid peroxidation (Sharma et al, 2000;Chang et al, 2007). Stress causes hyperthermia in both humans (Marazziti et al, 1992) and rodents (Olivier et al, 2003), and chronic stress decreases endogenous antioxidants and mitochondrial function, increases NO production, and produces lipid peroxidation in rodents (Madrigal et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Chronic Stress Enhances the Corticosterone Response and Neurotoxicity to +3,4-Methylenedioxymethamphetamine (MDMA): The Role of Ambient Temperature

Johnson

Yamamoto

2010

J Pharmacol Exp Ther

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Stress facilitates drug abuse by humans. In rodents, stress enhances the neurochemical, neuroendocrine, and behavioral responses to psychostimulants. Although chronic unpredictable stress (CUS) enhances the acute hyperthermic and longterm monoamine-depleting effects of the psychostimulant ϩ3,4-methylenedioxymethamphetamine (MDMA), the roles of hyperthermia and corticosterone (CORT) in mediating the stress-induced enhancement of MDMA-induced serotonin (5-HT) and dopamine (DA) depletions are unknown. Rats were exposed to 10 days of CUS and then challenged with MDMA (5 mg/kg i.p. once every 2 h for a total of four injections). Prior exposure to CUS augmented MDMA-induced hyperthermia and plasma CORT secretion and the long-term depletions in 5-HT content in striatum, hippocampus, and frontal cortex and DA content in striatum. A reduced ambient temperature of 21°C attenuated the hyperthermia, CORT secretion, and 5-HT decreases after MDMA in nonstressed rats. The lower ambient temperature also prevented the augmented hyperthermia, CORT secretion, and enhanced 5-HT and DA depletions after MDMA in chronically stressed rats to levels exhibited by nonstressed, MDMA-treated rats. To investigate the role of CORT on monoamine depletions in response to MDMA, stressed and nonstressed rats were treated with the CORT synthesis inhibitor metyrapone during exposure to MDMA. Metyrapone prevented CORT secretion in both stressed and nonstressed rats but did not modify 5-HT or DA depletions in any brain region examined. This study suggests that enhanced CORT is a consequence of enhanced hyperthermia and the CUS-induced enhancements of MDMA-induced monoamine depletions may be mediated by hyperthermia but not CORT.

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Role of Nitric Oxide in Blood-Brain Barrier Permeability, Brain Edema and Cell Damage Following Hyperthermic Brain Injury. An Experimental Study Using EGB-761 and Gingkolide B Pretreatment in the Rat

Cited by 50 publications

References 14 publications

Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications

Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications

S-Nitrosoglutathione Induces Ciliary Neurotrophic Factor Expression in Astrocytes, Which Has Implications to Protect the Central Nervous System under Pathological Conditions

Chronic Stress Enhances the Corticosterone Response and Neurotoxicity to +3,4-Methylenedioxymethamphetamine (MDMA): The Role of Ambient Temperature

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