Cerebral Blood Volume in Acute Brain Infarction

Hatazawa, Jun; Shimosegawa, Eku; Toyoshima, Hideto; Ardekani, Babak A.; Suzuki, Akifumi; Okudera, Toshio; Miura, Yuko

doi:10.1161/01.str.30.4.800

Cited by 102 publications

(15 citation statements)

References 41 publications

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“…Cerebral blood volume has been previously reported to be, normal, increased, or decreased after acute brain ischemia, which appears to depend upon the severity of hypoperfusion (Hatazawa et al, 1999). However, there is no information available on changes in vascular volume after ischemia in fetal subjects treated with anti-IL-1β antibody infusions.…”

Section: Discussionmentioning

confidence: 99%

Neutralizing anti-interleukin-1β antibodies modulate fetal blood–brain barrier function after ischemia

Chen

Sadowska

Zhang

et al. 2015

Neurobiology of Disease

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We have previously shown that increases in blood-brain barrier permeability represent an important component of ischemia-reperfusion related brain injury in the fetus. Pro-inflammatory cytokines could contribute to these abnormalities in blood-brain barrier function. We have generated pharmacological quantities of mouse anti-ovine interleukin-1β monoclonal antibody and shown that this antibody has very high sensitivity and specificity for interleukin-1β protein. This antibody also neutralizes the effects of interleukin-1β protein in vitro. In the current study, we hypothesized that the neutralizing anti-interleukin-1β monoclonal antibody attenuates ischemia-reperfusion related fetal blood-brain barrier dysfunction. Instrumented ovine fetuses at 127 days of gestation were studied after 30 minutes of carotid occlusion and 24 hours of reperfusion. Groups were sham operated placebo-control- (n=5), ischemia-placebo- (n=6), ischemia-anti-IL-1β antibody- (n=7), and sham-control antibody- (n=2) treated animals. Systemic infusions of placebo (0.154 M NaCl) or anti-interleukin-1β monoclonal antibody (5.1±0.6 mg/kg) were given intravenously to the same sham or ischemic group of fetuses at 15 minutes and 4 hours after ischemia. Concentrations of interleukin-1β protein and anti-interleukin-1β monoclonal antibody were measured by ELISA in fetal plasma, cerebrospinal fluid, and parietal cerebral cortex. Blood-brain barrier permeability was quantified using the blood-to-brain transfer constant (Ki) with α-aminoisobutyric acid in multiple brain regions. Interleukin-1β protein was also measured in parietal cerebral cortices and tight junction proteins in multiple brain regions by Western immunoblot. Cerebral cortical interleukin-1β protein increased (P<0.001) after ischemia-reperfusion. After anti-interleukin-1β monoclonal antibody infusions, plasma anti-interleukin-1β monoclonal antibody was elevated (P<0.001), brain anti-interleukin-1β monoclonal antibody levels were higher (P<0.03), and interleukin-1β protein concentrations (P<0.03) and protein expressions (P<0.001) were lower in the monoclonal antibody-treated group than in placebo-treated-ischemia-reperfusion group. Monoclonal antibody infusions attenuated ischemia-reperfusion-related increases in Ki across the brain regions (P<0.04), and Ki showed an inverse linear correlation (r = −0.65, P<0.02) with anti-interleukin-1β monoclonal antibody concentrations in the parietal cortex, but had little effect on tight junction protein expression. We conclude that systemic anti-interleukin-1β monoclonal antibody infusions after ischemia result in brain anti-interleukin-1β antibody uptake, and attenuate ischemia-reperfusion-related interleukin-1β protein up-regulation and increases in blood-brain barrier permeability across brain regions in the fetus. The pro-inflammatory cytokine, interleukin-1β, contributes to impaired blood-brain barrier function after ischemia in the fetus.

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Section: Discussionmentioning

confidence: 99%

Neutralizing anti-interleukin-1β antibodies modulate fetal blood–brain barrier function after ischemia

Chen

Sadowska

Zhang

et al. 2015

Neurobiology of Disease

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“…The level of flow decrease that predicts extended infarction or hemorrhagic complications was estimated at different values and varied between complete lack of ECD uptake and a relative decrease in perfusion to 35–60% of the contralateral value [55,56,57]. The threshold for a moderately ischemic area with a good chance of recovery was set at 70% of contralateral tracer uptake in several studies [58, 59].…”

Section: Single-photon-emission Computed Tomographymentioning

confidence: 99%

The Concept of Ischemic Penumbra in Acute Stroke and Therapeutic Opportunities

Paciaroni

Caso²,

Agnelli³

2009

Eur Neurol

119

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Ischemic penumbra was first defined by Astrup in 1981 as perfused brain tissue at a level within the thresholds of functional impairment and morphological integrity, which has the capacity to recover if perfusion is improved. It exists, even for a short period of time in the center of ischemia, from which irreversible necrosis propagates to the neighboring tissues over time. Penumbra has become the focus of intense imaging research to differentiate it from infarction. Accurate detection of this ‘tissue at risk’ could be used to identify patients who would benefit most from acute treatment. Currently, recombinant tissue plasminogen activator (rtPA) is the only approved drug that has shown significant benefits in acute stroke patients when administered intravenously less than 4.5 h after stroke. However, its use is limited. Discrimination between infarct core and the surrounding potentially salvageable tissue is useful to better identify patients suitable for treatment. This can be achieved by positron emission tomography, single-photon-emission computed tomography, computed tomography perfusion scan and perfusion-weighted and diffusion-weighted magnetic resonance imaging. Identification of the penumbra might enable selective rtPA use in patients with large penumbras and small infarct cores, even beyond the 4.5-hour time window, where the penumbra may persist for more than 12 h. The purpose of this review was to describe neuroimaging modalities capable of identifying penumbra tissue so as to provide surrogate markers for new trials in acute ischemic stroke patients.

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“…4 We previously reported that total CBV severely decreased in ischemic core in acute stroke patients. 5 The mechanism responsible for upper limitation of OEF would be a restricted D c due to capillary blood volume reduction in ischemic brain. Objectives: QSPECT package has been developed for standardized calculation of quantitative CBF images using I-123 IMP 1 and is appropriate for multicenter clinical studies.…”

Section: Discussionmentioning

confidence: 99%

BrainPET Poster Session: Molecular Brain Imaging—Clinical Applications

2009

J Cereb Blood Flow Metab

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Objective: To explore glucose metabolism changes of refractory Gilles de la Tourette syndrome (GTS) in PET scan and observe the effect of stereotactic bilateral capsulotomy for refractory GTS patients. Methods: We examined the localized orbitofrontal and subcortical metabolic changes in FDG-PET by employing the region of interest (ROI) method in pre-operation and 6 months after operation. 7 cases refractory GTS underwent MRI guided stereotactic bilateral capsulotomy. The post-operation outcome of brain metabolic and clinical scales including tic severity, cognitive performance, and psychiatric status are under investigation by contrast to pre-operation so as to detect and evaluate the effects of capsulotomy for refractory GTS.Results: There was a remarkable difference between the patients and control team in regional glucose metabolic changes (P < 0.01). Moreover stereotactic capsulotomy induces localized orbitofrontal and subcortical metabolic changes and improves clinical symptoms in refractory GTS. No any serous side effects happened except transient urpclepsia and weight loss in our study. Conclusion:The metabolic abnormalities of FDG are universal and remarkable in PET to refractory GTS, especially in frontal Lobe, orbitofrontal lobe, cingulated cortices, and caudate. FDG-PET changes demonstrated that capsulotomy do decrease remarkably regional hypermetabolism, which might be related to mechanism of surgical treatment of refractory GTS. MRI guided stereotactic capsulotomy is a precise, safe, very effective therapy in some ways for refractory GTS. 57. Postoperative cortical neural loss associated with cerebral hyperperfusion and cognitive impairment after carotid endarterectomy: Background and aims: Although cerebral hyperperfusion after carotid endarterectomy (CEA) often impairs cognitive function, MRI does not always demonstrate structural brain damage associated with postoperative cognitive impairment. The purpose of the present study was to determine whether postoperative cortical neural loss, which can be detected by 123 I-iomazenil (IMZ) single-photon emission CT, is associated with cerebral hyperperfusion after CEA and whether it correlates with postoperative cognitive impairment. Methods: In 60 patients undergoing CEA for ipsilateral internal carotid artery stenosis ( > 70%), cerebral blood flow was measured using N-isopropylp-[ 123 I]-iodoamphetamine single-photon emission CT before and immediately after CEA and on the third postoperative day. The distribution of benzodiazepine receptor binding potential in the cerebral cortex was assessed using 123 I-iomazenilsingle-photon emission CT before and one month after surgery and was analyzed using three-dimensional stereotactic surface projection. Neuropsychological testing was also performed preoperatively and at the first postoperative month. Results: Post-CEA hyperperfusion and postoperative cognitive impairment were observed in 9 patients (15%) and 8 patients (13%), respectively. Post-CEA hyperperfusion was significantly associated with postoperat...

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Cerebral Blood Volume in Acute Brain Infarction

Cited by 102 publications

References 41 publications

Neutralizing anti-interleukin-1β antibodies modulate fetal blood–brain barrier function after ischemia

Neutralizing anti-interleukin-1β antibodies modulate fetal blood–brain barrier function after ischemia

The Concept of Ischemic Penumbra in Acute Stroke and Therapeutic Opportunities

BrainPET Poster Session: Molecular Brain Imaging—Clinical Applications

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