Brain Energy Metabolism in Patients With Spontaneous Subarachnoid Hemorrhage and Global Cerebral Edema

Zetterling, Maria; Hallberg, Lena; Hillered, Lars; Karlsson, Torbjörn; Enblad, Per; Engström, Elisabeth Ronne

doi:10.1227/01.neu.0000370893.04586.73

Cited by 42 publications

(38 citation statements)

References 47 publications

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“…Brain edema is one of the common and important features of both clinical SAH and experimental SAH [29,30]. Brain edema after SAH reflects disruption of the BBB, which is primarily induced by endothelial cells apoptosis, degradation of the basal-lamina by proteases, and diffuse inflammatory reaction [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Chen

et al. 2015

Mol Neurobiol

126

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Minocycline has beneficial effects in early brain injury (EBI) following subarachnoid hemorrhage (SAH); however, the molecular mechanisms underlying these effects have not been clearly identified. This study was undertaken to determine the influence of minocycline on inflammation and neural apoptosis and the possible mechanisms of these effects in early brain injury following subarachnoid hemorrhage. SAH was induced by the filament perforation model of SAH in male Sprague-Dawley rats. Minocycline or vehicle was given via an intraperitoneal injection 1 h after SAH induction. Minocycline treatment markedly attenuated brain edema secondary to blood-brain barrier (BBB) dysfunction by inhibiting NLRP3 inflammasome activation, which controls the maturation and release of pro-inflammatory cytokines, especially interleukin-1β (IL-1β). Minocycline treatment also markedly reduced the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells. To further identify the potential mechanisms, we demonstrated that minocycline increased Bcl2 expression and reduced the protein expression of P53, Bax, and cleaved caspase-3. In addition, minocycline reduced the cortical levels of reactive oxygen species (ROS), which are closely related to both NLRP3 inflammasome and P53 expression. Minocycline protects against NLRP3 inflammasome-induced inflammation and P53-associated apoptosis in early brain injury following SAH. Minocycline's anti-inflammatory and anti-apoptotic effect may involve the reduction of ROS. Minocycline treatment may exhibit important clinical potentials in the management of SAH.

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Section: Discussionmentioning

confidence: 99%

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Chen

et al. 2015

Mol Neurobiol

126

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“…As the disease worsens, there is a progressive decrease in the ability to perform ADL (Nici et al., 2006). Patients with cerebral edema develop cerebral hypermetabolism (Zetterling et al., 2010), which may increase the energy demand in the brain. Hypermetabolism is linked to disability and cognitive dysfunction (Claassen et al., 2002).…”

Section: Introductionmentioning

confidence: 99%

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

et al. 2018

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IntroductionThe aim of this study was to explore whether patients with chronic obstructive pulmonary disease (COPD) develop vasogenic cerebral edema, and whether this edema contributes to the COPD‐related disability.MethodsEighteen stable patients with COPD and 17 matched healthy volunteers were enrolled. Apparent diffusion coefficient (ADC) values were calculated by voxel‐based analysis using DTI‐Studio software based on diffusion tensor imaging. COPD‐related disability was calculated using activities of daily living (ADL) scale.ResultsIn patients with COPD, ADC increased in the white matter fiber tracts including the bilateral anterior cingulum and posterior corpus callosum and in the white matter fibers connecting the bilateral insular cortices, sub‐lobar cortices, and pars triangularis cortices and the left rectus and olfactory gyrus. However, after further controlling for cigarette smoking, the difference in ADC values in the posterior corpus callosum between groups disappeared. Patients with COPD had significantly higher scores in ADL than that in controls. Moreover, ADL scores were positively correlated with the increased regional ADC values.ConclusionVasogenic cerebral edema occurs in patients with COPD. Cigarette smoking may be a risk factor for COPD‐related vasogenic edema. Vasogenic cerebral edema may be related to the COPD‐related ADL impairment.

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“…A delayed pattern of hyperglycolysis has been observed in SAH patients and associated with favorable outcome, although those measurements were not done in the ultra-early phase. [22], [23] One problem with microdialysis is that it provides a focal measurement. However, in the present model we assumed that the change in CPP following the intervention produced global energy metabolic perturbation, presumably making our microdialysis data representative.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Pattern of the Acute Phase of Subarachnoid Hemorrhage in a Novel Porcine Model: Studies with Cerebral Microdialysis with High Temporal Resolution

et al. 2014

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BackgroundAneurysmal subarachnoid hemorrhage (SAH) may produce cerebral ischemia and systemic responses including stress. To study immediate cerebral and systemic changes in response to aneurysm rupture, animal models are needed.ObjectiveTo study early cerebral energy changes in an animal model.MethodsExperimental SAH was induced in 11 pigs by autologous blood injection to the anterior skull base, with simultaneous control of intracranial and cerebral perfusion pressures. Intracerebral microdialysis was used to monitor concentrations of glucose, pyruvate and lactate.ResultsIn nine of the pigs, a pattern of transient ischemia was produced, with a dramatic reduction of cerebral perfusion pressure soon after blood injection, associated with a quick glucose and pyruvate decrease. This was followed by a lactate increase and a delayed pyruvate increase, producing a marked but short elevation of the lactate/pyruvate ratio. Glucose, pyruvate, lactate and lactate/pyruvate ratio thereafter returned toward baseline. The two remaining pigs had a more severe metabolic reaction with glucose and pyruvate rapidly decreasing to undetectable levels while lactate increased and remained elevated, suggesting persisting ischemia.ConclusionThe animal model simulates the conditions of SAH not only by deposition of blood in the basal cisterns, but also creating the transient global ischemic impact of aneurysmal SAH. The metabolic cerebral changes suggest immediate transient substrate failure followed by hypermetabolism of glucose upon reperfusion. The model has features that resemble spontaneous bleeding, and is suitable for future research of the early cerebral and systemic responses to SAH that are difficult to study in humans.

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Brain Energy Metabolism in Patients With Spontaneous Subarachnoid Hemorrhage and Global Cerebral Edema

Cited by 42 publications

References 47 publications

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

Metabolic Pattern of the Acute Phase of Subarachnoid Hemorrhage in a Novel Porcine Model: Studies with Cerebral Microdialysis with High Temporal Resolution

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