Peripheral to central: Organ interactions in stroke pathophysiology

Ma, Shubei; Zhao, Haiping; Ji, Xunming; Luo, Yumin

doi:10.1016/j.expneurol.2015.05.014

Cited by 34 publications

(28 citation statements)

References 128 publications

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“…Brain ischaemia leads to central cellular injury but it also influences several peripheral organs, via, for example, the immune and/or the nervous systems (Ma et al . ). In the GI tract, a disrupted mucosal barrier (Feng et al .…”

Section: Discussionmentioning

confidence: 97%

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Focal, but not global, cerebral ischaemia causes loss of myenteric neurons and upregulation of vasoactive intestinal peptide in mouse ileum

Cheng

Svensson

Yang

et al. 2018

Int J Experimental Path

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Reduced blood flow to the brain induces cerebral ischaemia, potentially causing central injury and peripheral complications including gastrointestinal (GI) dysfunction. The pathophysiology behind GI symptoms is suspected to be neuropathy in the enteric nervous system (ENS), which is essential in regulating GI function. This study investigates if enteric neuropathy occurs after cerebral ischaemia, by analysing neuronal survival and relative numbers of vasoactive intestinal peptide (VIP) and neuronal nitric oxide synthase (nNOS) expressing neurons in mouse ileum after three types of cerebral ischaemia. Focal cerebral ischaemia, modelled by permanent middle cerebral artery occlusion (pMCAO) and global cerebral ischaemia, modelled with either transient occlusion of both common carotid arteries followed by reperfusion (GCIR) or chronic cerebral hypoperfusion (CCH) was performed on C56BL/6 mice. Sham-operated mice for each ischaemia model served as control. Ileum was collected after 1-17 weeks, depending on model, and analysed using morphometry and immunocytochemistry. For each group, intestinal mucosa and muscle layer thicknesses, neuronal numbers and relative proportions of neurons immunoreactive (IR) for nNOS or VIP were estimated. No alterations in mucosa or muscle layer thicknesses were noted in any of the groups. Loss of myenteric neurons and an increased number of VIP-IR submucous neurons were found in mouse ileum 7 days after pMCAO. None of the global ischaemia models showed any alterations in neuronal survival or relative numbers of VIP- and nNOS-IR neurons. We conclude that focal cerebral ischaemia and global cerebral ischaemia influence enteric neuronal survival differently. This is suggested to reflect differences in peripheral neuro-immune responses.

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Section: Discussionmentioning

confidence: 97%

“…; Ma et al . ). Studies on the mechanisms behind central ischaemia‐induced intestinal dysfunction indicate mucosal barrier disruption (Feng et al .…”

mentioning

confidence: 97%

Focal, but not global, cerebral ischaemia causes loss of myenteric neurons and upregulation of vasoactive intestinal peptide in mouse ileum

Cheng

Svensson

Yang

et al. 2018

Int J Experimental Path

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“…The occurrence of stroke can directly affect the kidney by activating the renal sympathetic nervous system that modulates renal blood flow and glomerular filtration, by releasing vasopressin and causing imbalances in sodium and water [6,4]. Furthermore, clinical studies have shown that renal dysfunction can predict adverse outcomes in patients with stroke [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Incidence, Risk factors, and Biomarkers Predicting Ischemic or Hemorrhagic Stroke Associated Acute Kidney Injury and Outcome: A Retrospective Study in a General Intensive Care Unit

Jiang

Xiang

et al. 2019

Blood Purif

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Objective: We investigated the epidemiology, risk factors, and predictive parameters for ischemic or hemorrhagic stroke-associated acute kidney injury (AKI) and mortality in a general intensive care unit (ICU) in China. Methods: During 5 years, 479 stroke patients were screened, and 381 were enrolled. AKI was diagnosed within 7 days after ICU admission, based on the Kidney Disease Improving Global Outcomes criteria. Risk factors of AKI were assessed by Logistic regression analyses, and the predictive biomarkers for AKI were determined using receiver operating characteristic (ROC) curves. Also examined were factors influencing 28-day mortality, using Cox regression analyses and Kaplan-Meier curves. Results: Among all, 115 (30.18%) patients developed AKI. Multivariate regression analyses revealed that the following features at ICU admission significantly increased the risk of developing AKI: an increased National Institutes of Health Stroke Scale score (OR 1.136, p < 0.001) and Acute Physiology and Chronic Health Evaluation II score (OR 1.107, p = 0.042); hypertension (OR 2.346, p = 0.008); use of loop diuretics (OR 1.961, p = 0.032); and higher serum cystatin C (sCysC; OR 8.156, p = 0.001). The area under the ROC curves for predicting AKI using sCysC was 0.772, slightly better than that of other biomarkers. The sCysC ≥0.93 mg/L (hazard ratio 1.844, p = 0.004) significantly predicted 28-day mortality. Conclusions: Among stroke patients in ICU, we identified significant risk factors of stroke-associated AKI. Serum CysC level at ICU admission was an important biomarker for predicting AKI and 28-day mortality.

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“…This region does not affect directly with ischemic stroke rats induced by MCAO but it is known that the function of the human body depends on the interaction of all organs, and brain damage resulting from a stroke can lead to multiple organ failures especially in cerebellum brain area [12]. The correlation between MCAO and cerebellum was not fully understood.…”

mentioning

confidence: 99%

“…These processes induce neuron damaging. In contrast, the hypoxia caused by blood flow blocking triggers a protein stress to form Heat Shock Protein-90 (HSP-90) [12]. This protein stimulates BDNF activation through activation of protein kinase B and Adenine Monophosphate-Activated Protein Kinase (AMPK)/ERK [13].…”

mentioning

confidence: 99%

Potential of Anthocyanin From Purple Sweet Potato (Ipomoea batatas) To Increase BDNF Level and VEGF Expression in The Cerebellum of Ischemic Stroke Rats

Wati

Prasetyawan

Mahdi

et al. 2018

J. Pure App. Chem. Res.

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This paper reports the effect of anthocyanin from purple sweet potato in the cerebellum of ischemic stroke rats model by Middle Cerebral Artery Occlusion (MCAO) technique. This technique was carried out by ligating the blood flow in External Carotid Artery (ECA), Common Carotid Artery (CCA) and Internal Carotid Artery (ICA) for 3 hours, followed by reperfusion. The MCAO technique proved a technique for preparing ischemic stroke rats. This technique induces releasing of Brain-Derived Nuclear Factor (BDNF) and Vascular Endothelial Growth Factor (VEGF) in the cerebellum of ischemic stroke rats. The levels of BDNF measured by ELISA technique and VEGF expression used immunohistochemistry technique. The results showed that anthocyanin from purple sweet potato increases the level of both BDNF and VEGF expression in the cerebellum of ischemic stroke rats. It is suggested that anthocyanin could be used as a therapeutic agent for ischemic stroke.

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Peripheral to central: Organ interactions in stroke pathophysiology

Cited by 34 publications

References 128 publications

Focal, but not global, cerebral ischaemia causes loss of myenteric neurons and upregulation of vasoactive intestinal peptide in mouse ileum

Focal, but not global, cerebral ischaemia causes loss of myenteric neurons and upregulation of vasoactive intestinal peptide in mouse ileum

Incidence, Risk factors, and Biomarkers Predicting Ischemic or Hemorrhagic Stroke Associated Acute Kidney Injury and Outcome: A Retrospective Study in a General Intensive Care Unit

Potential of Anthocyanin From Purple Sweet Potato (Ipomoea batatas) To Increase BDNF Level and VEGF Expression in The Cerebellum of Ischemic Stroke Rats

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