Influence of surgical pain stress on the blood-brain barrier permeability in rats

Öztaş, Baria; Akgul, Sibel; Arslan, Ferhat

doi:10.1016/j.lfs.2003.07.054

Cited by 21 publications

(10 citation statements)

References 23 publications

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“…Also, delirium during the early phases of septic shock is associated with leucoencephalopathy in brain magnetic resonance imaging (MRI), suggestive of BBB breakdown [119]. In addition to systemic inflammation, other factors affect the BBB microscopic structure and function, including hypoxia, ischaemia and pain [93,104]. Conditions where these factors occur simultaneously (e.g.…”

Section: Disruption Of Blood-brain Barriermentioning

confidence: 99%

The neuroinflammatory hypothesis of delirium

et al. 2010

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Delirium is a neuropsychiatric syndrome characterized by a sudden and global impairment in consciousness, attention and cognition. It is particularly frequent in elderly subjects with medical or surgical conditions and is associated with short-and long-term adverse outcomes. The pathophysiology of delirium remains poorly understood as it involves complex multi-factorial dynamic interactions between a diversity of risk factors. Several conditions associated with delirium are characterized by activation of the inflammatory cascade with acute release of inflammatory mediators into the bloodstream. There is compelling evidence that acute peripheral inflammatory stimulation induces activation of brain parenchymal cells, expression of proinflammatory cytokines and inflammatory mediators in the central nervous system. These neuroinflammatory changes induce neuronal and synaptic dysfunction and subsequent neurobehavioural and cognitive symptoms. Furthermore, ageing and neurodegenerative disorders exaggerate microglial responses following stimulation by systemic immune stimuli such as peripheral inflammation and/or infection. In this review we explore the neuroinflammatory hypothesis of delirium based on recent evidence derived from animal and human studies.

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Section: Disruption Of Blood-brain Barriermentioning

confidence: 99%

The neuroinflammatory hypothesis of delirium

et al. 2010

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“…However, mixed results have been reported with some studies reporting that prolonged exposure to stress can affect the increases in BBB permeability 34 , 35 and others reporting no effect of chronic stress on BBB permeability 33 , 36 , 37 . Most studies that have investigated the correlation between stress and BBB permeability have used an endpoint assay, i.e., extravasation of Evans blue or sodium fluorescein shown with tissue slice imaging and colorimetric quantification 31 , 33 , 38 , 39 . These methods may incorrectly overestimate the signal of Evans blue or sodium fluorescein in tissue due to insufficient perfusion power to remove all residual dyes in blood vessels 31 .…”

Section: Introductionmentioning

confidence: 99%

Real-time in vivo two-photon imaging study reveals decreased cerebro-vascular volume and increased blood-brain barrier permeability in chronically stressed mice

Lee

Kang

Kim

et al. 2018

Sci Rep

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Chronic stress disrupts brain homeostasis and adversely affects the cerebro-vascular system. Even though the effects of chronic stress on brain system have been extensively studied, there are few in vivo dynamic studies on the effects of chronic stress on the cerebro-vascular system. In this study, the effects of chronic stress on cerebral vasculature and BBB permeability were studied using in vivo two-photon (2p) microscopic imaging with an injection of fluorescence-conjugated dextran. Our real-time 2p imaging results showed that chronic stress reduced the vessel diameter and reconstructed vascular volume, regardless of vessel type and branching order. BBB permeability was investigated with two different size of tracers. Stressed animals exhibited a greater BBB permeability to 40-kDa dextran, but not to 70-kDa dextran, which is suggestive of weakened vascular integrity following stress. Molecular analysis revealed significantly higher VEGFa mRNA expression and a reduction in claudin-5. In summary, chronic stress decreases the size of cerebral vessels and increases BBB permeability. These results may suggest that the sustained decrease in cerebro-vascular volume due to chronic stress leads to a hypoxic condition that causes molecular changes such as VEGF and claudin-5, which eventually impairs the function of BBB.

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“…Stresses are strong physical pressures applied to an object. Many stressors exist such as immobilization (Nankova et al ., 1996), electric shock (Chida et al ., 2004), pain stress (Oztaş et al ., 2004) and cold water stress (Feng et al ., 2005). Among those stressors, immobilization and electric shock are commonly used and they are easy to implement.…”

Section: Introductionmentioning

confidence: 99%

Enhancement of Anxiety and Modulation of TH and pERK Expressions in Amygdala by Repeated Injections of Corticosterone

Lim

Jang²,

Lee³

et al. 2012

Biomolecules and Therapeutics

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Repeated stress induces corticosterone release. However, it is not clear that stress results in further elevation of corticosterone levels, and the roles of released corticosterone to aggravate stress-related symptoms are also not clear. This study investigated whether neuronal modulation was induced in the amygdala after two kinds of stress, that is, such as electric shock and corticosterone injection. It was found that stress by electric shock decreased the expression of tyrosine hydoroxylase (TH) in the amygdala while the expression of pERK was increased. However, there is no difference in the expressions of TH and pERK in the frontal cortex compared with those of the control group. The level of corticosterone was significantly increased in the serum after stress. To determine the effect of corticosterone on the induction of anxiety and the expression of TH, the rats received corticosterone (20 mg or 40 mg/kg i.p.) for 1 day, 1 week, 2 weeks and 3 weeks, respectively. The spent time in open arms of the EPM (elevated plus maze) test was significantly decreased after 1 week, 2 weeks and 3 weeks. The time spent in open arms of the EPM test after repeated injections of corticosterone was significantly decreased in a dose-dependent manner. The expression of TH in the amygdala was reduced after following repeated corticosterone treatment for 2 weeks and 3 weeks. Collectively, this study suggests that corticosterone has a major role in the induction of anxiety and the modulation of TH expression, at least, in the amygdala.

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Influence of surgical pain stress on the blood-brain barrier permeability in rats

Cited by 21 publications

References 23 publications

The neuroinflammatory hypothesis of delirium

The neuroinflammatory hypothesis of delirium

Real-time in vivo two-photon imaging study reveals decreased cerebro-vascular volume and increased blood-brain barrier permeability in chronically stressed mice

Enhancement of Anxiety and Modulation of TH and pERK Expressions in Amygdala by Repeated Injections of Corticosterone

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