Amino acids and thiobarbituric acid reactive substances in cerebrospinal fluid and plasma of patients with septic encephalopathy

Takezawa, Jun; Taenaka, Nobuyuki; Nishijima, Masako K.; Hirata, Toshifumi; Okada, Toshiki; Shimada, Yasuhiro; Yoshiya, Ikuto

doi:10.1097/00003246-198311000-00007

Cited by 25 publications

(14 citation statements)

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“…In contrast to our findings, clinical studies have reported that the cerebrospinal fluid concentration of phenylalanine is elevated in septic patients (Takezawa et al ., ; Mizock et al ., ), which is also supported by findings from animal studies (Freund et al ., , ). The absence of any increase in phenylalanine in our study may, however, be related to a substantial variability in the reported transcerebral net exchange values and estimated changes in brain extracellular concentrations.…”

Section: Discussionsupporting

confidence: 84%

A reassessment of the blood–brain barrier transport of large neutral amino acids during acute systemic inflammation in humans

Berg

Taudorf

Bailey

et al. 2017

Clin Physio Funct Imaging

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We reassessed data from a previous study on the transcerebral net exchange of large neutral amino acids (LNAAs) using a novel mathematical model of blood-brain barrier (BBB) transport. The study included twelve healthy volunteers who received a 4-h intravenous lipopolysaccharide (LPS) infusion (total dose: 0·3 ng/kg), a human experimental model of the systemic inflammatory response during the early stages of sepsis. Cerebral blood flow and arterial-to-jugular venous LNAA concentrations were measured prior to and after LPS, and the BBB transport and brain extracellular concentrations of LNAAs were calculated. The arterial concentration and unidirectional cerebral influx of phenylalanine increased after LPS. The BBB transport of tyrosine was unaffected, while its concentration in the brain extracellular fluid increased. These findings suggest that LPS infusion leads to an increased cerebral uptake of phenylalanine, which is then metabolized to tyrosine. This may reflect a neuroprotective mechanism that 'detoxifies' excess intracerebral phenylalanine in the clinical setting of sepsis.

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Section: Discussionsupporting

confidence: 84%

A reassessment of the blood–brain barrier transport of large neutral amino acids during acute systemic inflammation in humans

Berg

Taudorf

Bailey

et al. 2017

Clin Physio Funct Imaging

View full text Add to dashboard Cite

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“…Malondialdehyde belongs to the group of thiobarbituric acid reactive substances (TBARS), meaning that it is capable of reacting with thiobarbituric acid to yield a fluorescent product than can be detected ex vivo (Moore and Roberts, 1998). The concentration of TBARS increases in cerebrospinal fluid of patients with sepsis (Takezawa et al, 1983) and in the brain homogenates of septic animals (Takeda et al, 1986;Abd El-Gawad and Khalifa, 2001;Sener et al, 2005a, b;Goraca and Aslanowicz-Antkowiak, 2009 demonstrated in specific brain regions, that is, the hippocampus, the cerebral cortex, and the cerebellum, as early as 6 hours after the induction of experimental sepsis in rats (Barichello et al, 2006).…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Neuro-oxidative-nitrosative stress in sepsis

Berg

Møller

Bailey

2011

J Cereb Blood Flow Metab

140

109

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Neuro-oxidative-nitrosative stress may prove the molecular basis underlying brain dysfunction in sepsis. In the current review, we describe how sepsis-induced reactive oxygen and nitrogen species (ROS/RNS) trigger lipid peroxidation chain reactions throughout the cerebrovasculature and surrounding brain parenchyma, due to failure of the local antioxidant systems. ROS/RNS cause structural membrane damage, induce inflammation, and scavenge nitric oxide (NO) to yield peroxynitrite (ONOO À ). This activates the inducible NO synthase, which further compounds ONOO À formation. ROS/RNS cause mitochondrial dysfunction by inhibiting the mitochondrial electron transport chain and uncoupling oxidative phosphorylation, which ultimately leads to neuronal bioenergetic failure. Furthermore, in certain 'at risk' areas of the brain, free radicals may induce neuronal apoptosis. In the present review, we define a role for ROS/RNS-mediated neuronal bioenergetic failure and apoptosis as a primary mechanism underlying sepsis-associated encephalopathy and, in sepsis survivors, permanent cognitive deficits.

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“…A septicemia, um estado comumente associado ao delirium, resulta em níveis elevados de fenilalanina (Takezawa et al, 1983). Uma elevação pré-operatória da proporção de fenilalanina com relação aos outros aminoácidos de cadeia larga foi reportado ser fator preditivo independente de delirium pós-cirurgia cardíaca, e maior proporção de fenilalanina com relação aos outros aminoácidos de cadeia larga, também, estava associada com delirium (van der Mast et al, 1996).…”

Section: Serotonina E Aminoácidos De Cadeia Largaunclassified

Mecanismos fisiopatológicos do delirium

Santos¹

2005

Rev. psiquiatr. clín.

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ResumoO delirium é uma das síndromes mais fascinantes na medicina, apesar de pobremente compreendida. Apesar de sua ocorrência freqüente e de haver crescente informação sobre o diagnóstico, fenomenologia, epidemiologia e etiologias, estudos sobre os mecanismos que mediam a fisiopatologia são, freqüentemente, ausentes. O desenvolvimento de sofisticadas metodologias de imagem cerebral tem permitido ir além das considerações diagnósticas e investigar a neurobiologia dos sintomas específicos observados no delirium. Esses avanços na neuropsiquiatria e na neuroimagem têm revelado diferenças entre as regiões cerebrais, incluindo os hemisférios. O delirium é uma síndrome que pode ocorrer como o resultado de múltipla e complexa interação entre sistemas de neurotransmissores e processos patológicos. Os neurotransmissores, acetilcolina e serotonina, podem ter participação importante no delirium devido a condições clínicas comuns, bem como no delirium pós-cirúrgico. Outros neurotransmissores (dopamina e GABA) e fatores neurobiológicos tais como citocinas, hormônios e radicais livres precisarão de mais estudos para definir as suas participações na gênese do delirium. Futuros estudos, centralizados na fisiopatologia do delirium, poderão levar a melhores estratégias de prevenção e tratamento.Palavras-chave: Delirium, estado confusional, transtorno mental orgânico, fisiopatologia. AbstractDelirium is one of the most fascinating and poorly understood syndromes in medicine. Despite its frequent occurrence and growing information on diagnosis, phenomenology, epidemiology, and aetiologies, studies on mediating pathophysiological mechanisms in delirium are largely lacking. The emergence of sophisticated brain imaging methodologies has made it possible to move beyond diagnostic consideration and investigate the neurobiology of specific symptom clusters observed in delirium. Advances in neuropsychiatry and neuroimaging have revealed differences between brain regions, including the hemispheres. Delirium is a syndrome that may occur as the result of multiple complex interacting neurotransmitter systems and pathologic processes. The

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Amino acids and thiobarbituric acid reactive substances in cerebrospinal fluid and plasma of patients with septic encephalopathy

Cited by 25 publications

References 0 publications

A reassessment of the blood–brain barrier transport of large neutral amino acids during acute systemic inflammation in humans

A reassessment of the blood–brain barrier transport of large neutral amino acids during acute systemic inflammation in humans

Neuro-oxidative-nitrosative stress in sepsis

Mecanismos fisiopatológicos do delirium

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