Brain edema in diseases of different etiology

Adeva, María M.; Souto, Gema; Donapetry, Cristóbal; Portals, Manuel; Rodríguez, Alberto Domínguez; Lamas, David

doi:10.1016/j.neuint.2012.05.007

Cited by 21 publications

(17 citation statements)

References 102 publications

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“…When the elevation of red-cell 2,3-bisphosphoglycerate is not appropriate (as in the case of hypophosphatemia), the tissue oxygen demand is no longer met by the oxygen delivery. This results in a massive capillary vasodilation with increased vascular permeability and plasma leakage into the interstitium with consequent oedema, affecting the brain and lungs [38].…”

Section: Comparative Analysismentioning

confidence: 99%

Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis

Yaneva

Константинова

Iliev

2016

Biotechnology & Biotechnological Equipment

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Cerebral oedema (CO) is a rare life-threatening complication of diabetic ketoacidosis (DKA) in children. We analysed the biochemical and therapeutic risk factors for CO in DKA by a retrospective review of 256 children hospitalized for DKA between February 2003 and March 2015. The demographic characteristics, biochemical variables and therapeutic interventions were compared between the patients with and without CO. CO was observed in 22 (8.6%) of the 256 subjects included in the study. One of these patients (5%) had a fatal outcome and two patients (9%) survived with neurological consequences. CO was significantly associated with severe DKA: lower initial venous pH (p < 0.001) and bicarbonate (p < 0.001), higher initial blood glucose (p < 0.01), urea level (p < 0.05) and baseline serum osmolality (p < 0.05). During the treatment of DKA, low serum phosphate level was found to be significantly associated with CO (p < 0.05). We also found significant dependence between the development of CO and the initiation of treatment for DKA in another facility before hospitalization in our hospital (p < 0.05), bicarbonate application (p < 0.001), higher fluid volume infused initially (p < 0.01) and delayed potassium substitution (p < 0.01). Severe ketoacidosis, hyperglycaemia and dehydration at presentation, and low serum phosphate during treatment are significantly related to CO formation in children with DKA. The initial severe acidosis and hyperglycaemia probably cause brain injury which progresses into CO in the course of developing hypophosphatemia and cerebral hypervolemia.

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Section: Comparative Analysismentioning

confidence: 99%

Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis

Yaneva

Константинова

Iliev

2016

Biotechnology & Biotechnological Equipment

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“…Due to its high metabolic rate, the brain requires more oxygen and glucose than other organs and is extremely vulnerable to ischemia or hypoxia resulting from decreased cerebral blood flow (CBF), increased intracranial pressure (ICP) and/or swelling and edema (2). Cerebral edema is a fairly common pathophysiological entity among TBI patients and is defined as an excess accumulation of water in the intra-and/or extra-cellular spaces of the brain, which can be induced by vasogenic, cytotoxic or osmotic factors (1,(5)(6)(7). TBI may result in interstitial (vasogenic) and intracellular (cytotoxic) edema, which contribute to secondary injury (1)(2)(3)7).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, it is crucial to protect hippocampal cells from the insult of ischemia, hypoxia and edema, in order to improve the outcome of TBI. Aquaporins (AQPs) are water channels that provide the major route for water movement across plasma membranes in a variety of tissues, including the brain (6,(15)(16)(17)(18)(19)(20). As a member of the AQPs, AQP-1 has been found to be expressed in astrocytes in cerebral edema associated with TBI, indicating an intimate connection between AQP-1 and cerebral edema (21).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of aquaporin-1 aggravates hippocampal damage in mouse traumatic brain injury models

Qiu

Sun

et al. 2014

Molecular Medicine Reports

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'Secondary insult' following primary traumatic brain injury (TBI), including ischemia and edema, may aggravate brain impairments and affect the outcomes. The hippocampus is particularly sensitive to ischemia or edema due to its selective vulnerability, as neural cells of the hippocampus may be more prone to abnormal function or cell death in response to ischemia and edema. Aquaporin‑1 (AQP‑1) was reported to be associated with cerebral edema; however, the expression and role of AQP‑1 in hippocampal edema following TBI have seldom been investigated. In the current study, BALB/c mouse closed craniocerebral injury models were established and the changes of AQP‑1 expression in hippocampi of mouse models following TBI were investigated. Neurological function and edema formation of the models were evaluated and the apoptotic hippocampal cells were then stained in situ and detected, followed by determination of AQP‑1 expression in the hippocampus using immunohistochemistry and western blot analysis. As a result, the majority of mice in the TBI group were severely injured and hippocampal edema was confirmed. The apoptotic cells increased significantly in the hippocampi of mice in the TBI group compared with those in the sham group (P<0.01) and the apoptotic rate increased gradually in a time‑dependent manner. The expression levels of AQP‑1 in the hippocampi of mice were markedly higher in the TBI group than in the sham group (P<0.05) at various time points and AQP‑1 expression levels peaked one day following TBI. These results indicate that upregulation of AQP‑1 may participate in edema formation and delayed cell death of the hippocampus following TBI and may also be a novel therapeutic target to protect the hippocampus from secondary injury following TBI.

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“…It is well established that hypoxia and hypercapnia, especially if they are sustained, may result in the development of brain edema (1,250). Although the pathomechanism of H/Hinduced brain edema is complex (257), cerebral vasodilation and the consequent increase of the hydrostatic pressure in brain capillaries is likely to play a key role in it.…”

Section: Cerebrovascular Actions Of Exogenous and Endogenous Cannabinmentioning

confidence: 99%

Endocannabinoids in cerebrovascular regulation

Benyó

Ruisanchez

Leszl-Ishiguro

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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The cerebral blood flow is tightly regulated by myogenic, endothelial, metabolic, and neural mechanisms under physiological conditions, and a large body of recent evidence indicates that inflammatory pathways have a major influence on the cerebral blood perfusion in certain central nervous system disorders, like hemorrhagic and ischemic stroke, traumatic brain injury, and vascular dementia. All major cell types involved in cerebrovascular control pathways (i.e., smooth muscle, endothelium, neurons, astrocytes, pericytes, microglia, and leukocytes) are capable of synthesizing endocannabinoids and/or express some or several of their target proteins [i.e., the cannabinoid 1 and 2 (CB1 and CB2) receptors and the transient receptor potential vanilloid type 1 ion channel]. Therefore, the endocannabinoid system may importantly modulate the regulation of cerebral circulation under physiological and pathophysiological conditions in a very complex manner. Experimental data accumulated since the late 1990s indicate that the direct effect of cannabinoids on cerebral vessels is vasodilation mediated, at least in part, by CB1 receptors. Cannabinoid-induced cerebrovascular relaxation involves both a direct inhibition of smooth muscle contractility and a release of vasodilator mediator(s) from the endothelium. However, under stress conditions (e.g., in conscious restrained animals or during hypoxia and hypercapnia), cannabinoid receptor activation was shown to induce a reduction of the cerebral blood flow, probably via inhibition of the electrical and/or metabolic activity of neurons. Finally, in certain cerebrovascular pathologies (e.g., subarachnoid hemorrhage, as well as traumatic and ischemic brain injury), activation of CB2 (and probably yet unidentified non-CB1/non-CB2) receptors appear to improve the blood perfusion of the brain via attenuating vascular inflammation. cerebral circulation; endocannabinoids; cannabinoid receptors; TRPV1 channel; neurovascular unit THE CEREBRAL VASCULATURE HAS two main homeostatic functions: 1) to adjust the local blood supply to the eventually rapidly changing metabolic demands of neurons; and 2) to maintain an optimal extracellular environment in the brain. The former function is realized by the regulation of the local cerebral blood flow (CBF), whereas the latter is achieved by the maintenance of the blood-brain barrier (BBB) and related transport mechanisms. The endocannabinoid system has been implicated as an important regulatory component in both of these cerebrovascular functions. The roles of endocannabinoids and cannabinoid receptors in the BBB have been reviewed recently (237). Here we aim to overview our knowledge on the endocannabinoid-mediated regulation of cerebral circulation.

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Brain edema in diseases of different etiology

Cited by 21 publications

References 102 publications

Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis

Risk factors for cerebral oedema in children and adolescents with diabetic ketoacidosis

Overexpression of aquaporin-1 aggravates hippocampal damage in mouse traumatic brain injury models

Endocannabinoids in cerebrovascular regulation

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