Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats

Thal, Serge C.; Sporer, Sonja; Kłopotowski, Mariusz; Thal, Simone E.; Woitzik, Johannes; Schmid-Elsaesser, Robert; Plesnila, Nikolaus; Zausinger, Stefan

doi:10.3171/2009.3.jns08412

Cited by 39 publications

(28 citation statements)

References 43 publications

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“…We found that rats that received ATX treatment at 30 minutes or 3 hours post-SAH showed a better neurological score at the early period, but not at 72 hours after SAH. In a previous study, Thal and colleagues 28 reported that brain edema formation instead of neuronal cell loss may be the major contributor to neurological dysfunction in the acute phase following SAH. Consistent with their conclusion, the neurological dysfunction observed in our experiment also showed a strong correspondence with the degree of brain edema, but not neuronal cell loss, in the early period after SAH.…”

Section: Discussionmentioning

confidence: 98%

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Zhang

Zhou

et al. 2014

JNS

103

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Object Aneurysmal subarachnoid hemorrhage (SAH) causes devastating rates of mortality and morbidity. Accumulating studies indicate that early brain injury (EBI) greatly contributes to poor outcomes after SAH and that oxidative stress plays an important role in the development of EBI following SAH. Astaxanthin (ATX), one of the most common carotenoids, has a powerful antioxidative property. However, the potential role of ATX in protecting against EBI after SAH remains obscure. The goal of this study was to assess whether ATX can attenuate SAH-induced brain edema, blood-brain barrier permeability, neural cell death, and neurological deficits, and to elucidate whether the mechanisms of ATX against EBI are related to its powerful antioxidant property. Methods Two experimental SAH models were established, including a prechiasmatic cistern SAH model in rats and a one-hemorrhage SAH model in rabbits. Both intracerebroventricular injection and oral administration of ATX were evaluated in this experiment. Posttreatment assessments included neurological scores, body weight loss, brain edema, Evans blue extravasation, Western blot analysis, histopathological study, and biochemical estimation. Results It was observed that an ATX intracerebroventricular injection 30 minutes post-SAH could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, neural cell apoptosis, and neurological dysfunction) after SAH in rats. Meanwhile, delayed treatment with ATX 3 hours post-SAH by oral administration was also neuroprotective in both rats and rabbits. In addition, the authors found that ATX treatment could prevent oxidative damage and upregulate the endogenous antioxidant levels in the rat cerebral cortex following SAH. Conclusions These results suggest that ATX administration could alleviate EBI after SAH, potentially through its powerful antioxidant property. The authors conclude that ATX might be a promising therapeutic agent for EBI following SAH.

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Section: Discussionmentioning

confidence: 98%

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Zhang

Zhou

et al. 2014

JNS

103

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“…Body weight was recorded daily as a general marker of well-being. A neuroscore (0 to 29 points, with 0 indicating no neurological deficit and 29 indicating severe neurological disability) was determined 1 day prior to and 24 and 72 h after SAH or sham surgery, as previously described [25,26]. Neuroscores were determined by an investigator blinded to the treatment.…”

Section: Ethics Animals and Housing Conditionsmentioning

confidence: 99%

Large Vessel Vasospasm Is Not Associated with Cerebral Cortical Hypoperfusion in a Murine Model of Subarachnoid Hemorrhage

Neulen

Meyer

Kramer

et al. 2018

Transl. Stroke Res.

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Clinical studies on subarachnoid hemorrhage (SAH) have shown discrepancies between large vessel vasospasm, cerebral perfusion, and clinical outcome. We set out to analyze the contribution of large vessel vasospasm to impaired cerebral perfusion and neurological impairment in a murine model of SAH. SAH was induced in C57BL/6 mice by endovascular filament perforation. Vasospasm was analyzed with microcomputed tomography, cortical perfusion by laser SPECKLE contrast imaging, and functional impairment with a quantitative neuroscore. SAH animals developed large vessel vasospasm, as shown by significantly lower vessel volumes of a 2.5-mm segment of the left middle cerebral artery (MCA) (SAH 5.6 ± 0.6 nL, sham 8.3 ± 0.5 nL, p < 0.01). Induction of SAH significantly reduced cerebral perfusion of the corresponding left MCA territory compared to values before SAH, which only recovered partly (SAH vs. sham, 15 min 35.7 ± 3.1 vs. 101.4 ± 10.2%, p < 0.01; 3 h, 85.0 ± 8.6 vs. 121.9 ± 13.4, p < 0.05; 24 h, 75.3 ± 4.6 vs. 110.6 ± 11.4%, p < 0.01; 72 h, 81.8 ± 4.8 vs. 108.5 ± 14.5%, n.s.). MCA vessel volume did not correlate significantly with MCA perfusion after 72 h (r = 0.34, p = 0.25). Perfusion correlated moderately with neuroscore (24 h: r = − 0.58, p < 0.05; 72 h: r = − 0.44, p = 0.14). There was no significant correlation between vessel volume and neuroscore after 72 h (r = − 0.21, p = 0.50). In the murine SAH model, cerebral hypoperfusion occurs independently of large vessel vasospasm. Neurological outcome is associated with cortical hypoperfusion rather than large vessel vasospasm.

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“…The tail artery was cannulated with a polyethylene tubing (PE50) for blood pressure monitoring. For ICP measurement, an intraparenchymal ICP probe (Codman) was advanced 2 mm into the brain [17]. After making a 4-cm skin incision over anterior midline neck, the right external and internal carotid arteries (ICA) were isolated.…”

Section: Experimental Sah Model and Physiologic Variable Monitoringmentioning

confidence: 99%

“…To evaluate the BBB integrity, Evans blue (EB) dye was used as a marker for albumin extravasation [24] at 24 h of SAH induction, when brain edema peaked [17]. Briefly, EB (2 % in saline, 4 ml/kg) was injected via the femoral vein and was allowed to remain in the circulation for 30 min.…”

Section: Evans Blue Assaymentioning

confidence: 99%

Memantine Alleviates Brain Injury and Neurobehavioral Deficits after Experimental Subarachnoid Hemorrhage

Huang

Wang

et al. 2014

Mol Neurobiol

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Subarachnoid hemorrhage (SAH) causes brain injury via glutamate excitotoxicity, which leads to an excessive Ca(2+) influx and this starts an apoptotic cascade. Memantine has been proven to reduce brain injury in several types of brain insults. This study investigated the neuro-protective potential of memantine after SAH and explored the underlying mechanisms. An endovascular perforation rat model of SAH was used and Sprague-Dawley rats were randomized into sham surgery, SAH + vehicle, and SAH + memantine groups. The effects of memantine on SAH were evaluated by assessing the neuro-behavioral functions, blood-brain barrier (BBB) permeability and neuronal cell preservation. The mechanisms of action of memantine, with its N-methyl-D-aspartate (NMDA) antagonistic characteristics on nitric oxide synthase (NOS) expression and peroxynitrite formation, were also investigated. The apoptotic cascade after SAH was suppressed by memantine. Neuronal NOS (nNOS) expression, peroxynitrite formation, and subsequent oxidative/nitrosative stress were also reduced. Memantine effectively preserved BBB integrity, rescued neuronal injury, and improved neurological outcome in experimental SAH. Memantine has neuro-protective potential in experimental SAH and may help combat SAH-induced brain damage in the future.

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Brain edema formation and neurological impairment after subarachnoid hemorrhage in rats

Cited by 39 publications

References 43 publications

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Large Vessel Vasospasm Is Not Associated with Cerebral Cortical Hypoperfusion in a Murine Model of Subarachnoid Hemorrhage

Memantine Alleviates Brain Injury and Neurobehavioral Deficits after Experimental Subarachnoid Hemorrhage

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