Emboli Formation Rather Than Inflammatory Mediators Are Responsible for Increased Cerebral Water Content After Conventional and Assisted Beating-Heart Myocardial Revascularization in a Porcine Model

Bierbach, Benjamin; Meier, Matthias; Kasper-König, W.; Heimann, Axel; Alessandri, Beat; Horstick, Georg; Oelert, H.; Kempski, Oliver

doi:10.1161/strokeaha.107.496620

Cited by 19 publications

(12 citation statements)

References 34 publications

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“…Nine studies seek to better understand the consequences of the CPB in microcirculation and inflammatory response, and all showed induction of inflammatory response and microcirculatory changes by CPB. The amount of activated leukocytes adhered to tissues and water in the extracellular space proved to be increased in the groups where CPB was performed, showing, respectively, activation of the inflammatory cascade and increased vascular permeability [ 4 - 6 ] . Moreover, it was found a significant reduction in blood flow and arteriolar endothelium-dependent relaxation [ 4 , 5 , 7 - 9 ] .…”

Section: Resultsmentioning

confidence: 99%

Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models

Liguori¹,

Kanas²,

Moreira³

2014

Revista Brasileira De Cirurgia Cardiovascular

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ObjectiveTo review studies performed in animal models that evaluated therapeutic interventions to inflammatory response and microcirculatory changes after cardiopulmonary bypass.MethodsIt was used the search strategy ("Cardiopulmonary Bypass" (MeSH)) and ("Microcirculation" (MeSH) or "Inflammation" (MeSH) or "Inflammation Mediators" (MeSH)). Repeated results, human studies, non-English language articles, reviews and studies without control were excluded.ResultsBlood filters, system miniaturization, specific primers regional perfusion, adequate flow and temperature and pharmacological therapies with anticoagulants, vasoactive drugs and anti-inflammatories reduced changes in microcirculation and inflammatory response.ConclusionDemonstrated efficacy in animal models establishes a perspective for evaluating these interventions in clinical practice.

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Section: Resultsmentioning

confidence: 99%

Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models

Liguori¹,

Kanas²,

Moreira³

2014

Revista Brasileira De Cirurgia Cardiovascular

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“…The tissues were then completely dried in an oven at 100°C for 5 days, and the dry weight of each hemisphere was recorded. The percentage of water content (% water) was calculated according to the Elliott formula [20]: %water = [(wet weight-dry weight)/wet weight]×100.…”

Section: Methodsmentioning

confidence: 99%

HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model

Yang

Wang

Yang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Traumatic brain injury (TBI) is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB), subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1) has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI. Methods: TBI was induced by controlled cortical impact (CCI) in adult male mice. HMGB1 A-box fragment was given intravenously at 2 mg/kg/day for 3 days after CCI. HMGB1 A-box-treated CCI mice were compared with saline-treated CCI mice and sham mice in terms of BBB disruption evaluated by Evan’s blue extravasation, brain edema by brain water content, cell death by propidium iodide staining, inflammation by Western blot and ELISA assay for cytokine productions, as well as neurological functions by the modified Neurological Severity Score, wire grip and beam walking tests. Results: HMGB1 A-box reversed brain damages in the mice following TBI. It significantly reduced brain edema by protecting integrity of the BBB, ameliorated cell degeneration, and decreased expression of pro-inflammatory cytokines released in injured brain after TBI. These cellular and molecular effects were accompanied by improved behavioral performance in TBI mice. Notably, HMGB1 A-box blocked IL-1β-induced HMGB1 release, and preferentially attenuated TLR4, Myd88 and P65 in astrocyte cultures. Conclusion: Our data suggest that HMGB1 is involved in CCI-induced TBI, which can be inhibited by HMGB1 A-box fragment. Therefore, HMGB1 A-box fragment may have therapeutic potential for the secondary brain damages in TBI.

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“…The tissues were completely dried in an oven at 100°C for 5 days, and the dry weight of each hemisphere was recorded. The percentage water content (% water) was calculated according to the Elliott formula for each hemisphere: [19].…”

Section: Methodsmentioning

confidence: 99%

Hydrogen Sulfide Offers Neuroprotection on Traumatic Brain Injury in Parallel with Reduced Apoptosis and Autophagy in Mice

et al. 2014

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Hydrogen sulfide (H2S), a novel gaseous mediator, has been recognized as an important neuromodulator and neuroprotective agent in the central nervous system. The present study was undertaken to study the effects of exogenous H2S on traumatic brain injury (TBI) and the underlying mechanisms. The effects of exogenous H2S on TBI were examined by using measurement of brain edema, behavior assessment, propidium iodide (PI) staining, and Western blotting, respectively. Compared to TBI groups, H2S pretreatment had reduced brain edema, improved motor performance and ameliorated performance in Morris water maze test after TBI. Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. The results suggest a protective effect and therapeutic potential of H2S in the treatment of brain injury and the protective effect against TBI may be associated with regulating apoptosis and autophagy.

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Emboli Formation Rather Than Inflammatory Mediators Are Responsible for Increased Cerebral Water Content After Conventional and Assisted Beating-Heart Myocardial Revascularization in a Porcine Model

Cited by 19 publications

References 34 publications

Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models

Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models

HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model

Hydrogen Sulfide Offers Neuroprotection on Traumatic Brain Injury in Parallel with Reduced Apoptosis and Autophagy in Mice

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