Multiparametric analysis of cerebral substrates and nitric oxide delivery in cerebrospinal fluid in patients with intracerebral haemorrhage: correlation with hemodynamics and outcome

Chiang, Ming-Fu; Chiu, Wen Ta; Lin, Fung-J; Thajeb, Peterus; Huang, Chia-Yu; Tsai, Shin Han

doi:10.1007/s00701-006-0771-z

Cited by 15 publications

(15 citation statements)

References 26 publications

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“…The glutamate content has been found to be clearly elevated in perihematomal brain tissue, and the prognosis of ICH is closely related with the EAA level [4,17,18].…”

Section: Discussionmentioning

confidence: 98%

“…Cerebral damage as a consequence of glutamate-mediated excitotoxicity is a major consequence of stroke. Recently published data confirmed the correlation between the level of excitatory amino acids (EAAs) and the outcome of ICHs, suggesting that neurochemical monitoring of these substances may have a role in the care of patients [4]. Glutamate-related excitotoxicity may have an important impact on secondary injury [1].…”

Section: Introductionmentioning

confidence: 95%

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Minimally Invasive Procedures for Evacuation of Intracerebral Hemorrhage Reduces Perihematomal Glutamate Content, Blood–Brain Barrier Permeability and Brain Edema in Rabbits

Wu¹,

Li²,

Wang³

et al. 2010

Neurocrit Care

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“…The glutamate content has been found to be clearly elevated in perihematomal brain tissue, and the prognosis of ICH is closely related with the EAA level [4,17,18].…”

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 95%

Minimally Invasive Procedures for Evacuation of Intracerebral Hemorrhage Reduces Perihematomal Glutamate Content, Blood–Brain Barrier Permeability and Brain Edema in Rabbits

Wu¹,

Li²,

Wang³

et al. 2010

Neurocrit Care

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“…Previous studies indicated that ICH increased the level of glutamate in the perihematomal area starting from 30 min, with a peak at 6 h to 12 h (Qureshi et al, 2003a, Nilsson et al, 2006). There was a 25-fold increase in the CSF glutamate level in ICH patients (Chiang et al, 2006). Glutamate induces the activation of the NMDA receptor (NMDAR) and leads to the formation of a complex of NMDAR-PSD95-nNOS.…”

Section: Discussionmentioning

confidence: 98%

“…It is known that intracerebral hemorrhage (ICH) increases the level of glutamate in the perihematomal area and in cerebral spinal fluid (CSF) during the acute phase of ICH (Chiang et al, 2006, Nilsson et al, 2006). In addition, blood and CSF glutamate concentrations independently predict a poor clinical outcome in ICH patients (Castillo et al, 2002, Chiang et al, 2006); however, whether elevated glutamate activates neuronal nitric oxide synthase (nNOS) in the ICH brain and whether nNOS is an important target for ICH treatment have not been previously investigated.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, blood and CSF glutamate concentrations independently predict a poor clinical outcome in ICH patients (Castillo et al, 2002, Chiang et al, 2006); however, whether elevated glutamate activates neuronal nitric oxide synthase (nNOS) in the ICH brain and whether nNOS is an important target for ICH treatment have not been previously investigated. nNOS is the main subtype of nitric oxide synthase in the brain (Zhou and Zhu, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Administration of S-methyl-l-thiocitrulline protects against brain injuries after intracerebral hemorrhage

Wagner

Broderick

et al. 2014

Neuroscience

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Although intracerebral hemorrhage (ICH) increases the level of glutamate in the perihematomal area and cerebral spinal fluid (CSF) in the ICH acute phase, it is unclear whether elevated glutamate activates neuronal nitric oxide synthase (nNOS) in the ICH brain and whether nNOS is an important target for ICH treatment. Here, we assessed the role of the nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) in the activity of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and ICH-induced brain injuries. An autologous blood intracerebral infusion model in male rats was used. All of the rats were sacrificed 24 hours after ICH. ICH increased NADPH-d activity in the striatum. Administering SMTC 3 h after ICH decreased the activity of NADH-d (p < 0.05 vs. the ICH group). The activation of gelatinolytic enzymes in the perihematomal region of the striatum was reduced by SMTC treatment (p < 0.01, vs. the ICH group). The loss of laminin- and occludin-stained vessels was significant in perihematomal regions after 24 h of ICH and was significantly attenuated by the administration of SMTC (p < 0.01 for laminin, p < 0.05 for occluding, compared with the ICH group). Neuronal death and neurological deficits after ICH were also decreased in SMTC treatment rats (p < 0.01, vs. the ICH group). The results suggest that the administration of the nNOS inhibitor SMTC after ICH protects against ICH-induced brain injuries and improves neurological function.

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Cerebrospinal fluid of brain trauma patients inhibits in vitro neuronal network function via NMDA receptors

Otto

Illes

Opatz

et al. 2009

Annals of Neurology

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Neurological diseases frequently induce pathological changes of cerebrospinal fluid (CSF) that might secondarily influence brain activity, as the CSF-brain barrier is partially permeable. However, functional effects of CSF on neuronal network activity have not been specified to date. Here, we report that CSF specimens from patients with reduced Glasgow Coma Scale values caused by severe traumatic brain injury suppress synchronous activity of in vitro-generated neuronal networks in comparison with controls. We present evidence that underlying mechanisms include increased N-methyl-D-aspartate receptor activity mediated by a CSF fraction containing elevated amino acid concentrations. These proof-of-principle data suggest that determining effects of CSF specimens on neuronal network activity might be of diagnostic value.

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Multiparametric analysis of cerebral substrates and nitric oxide delivery in cerebrospinal fluid in patients with intracerebral haemorrhage: correlation with hemodynamics and outcome

Abstract: This study confirms the correlation between the level of EAAs and the outcome of ICHs, suggesting that neurochemical monitoring of these substances may have a role in caring for patients.

Cited by 15 publications

References 26 publications

Minimally Invasive Procedures for Evacuation of Intracerebral Hemorrhage Reduces Perihematomal Glutamate Content, Blood–Brain Barrier Permeability and Brain Edema in Rabbits

Minimally Invasive Procedures for Evacuation of Intracerebral Hemorrhage Reduces Perihematomal Glutamate Content, Blood–Brain Barrier Permeability and Brain Edema in Rabbits

Administration of S-methyl-l-thiocitrulline protects against brain injuries after intracerebral hemorrhage

Cerebrospinal fluid of brain trauma patients inhibits in vitro neuronal network function via NMDA receptors

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