Matrix metalloproteinases are not involved in early brain edema formation after cardiac arrest in rats

Xiao, Feng; Arnold, Thomas C.; Zhang, S.; Imtiaz, Nauman; Khan, Anjum; Alexander, John; Conrad, Steven A.; Carden, Donna L.

doi:10.1007/978-3-7091-0651-8_17

Cited by 3 publications

(3 citation statements)

References 33 publications

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“…The CA1 subregion of the hippocampus is particularly susceptible to ischemia and exhibits delayed neuronal death 11,48 following acute ischemic insult. Matrix metalloproteinases, activated for several days following transient cerebral ischemia, 49,50 have been implicated in neuronal death in the hippocampal CA1 subregion. 51,52 ROS 53,54 and inflammatory mediators activate MMP following cerebral ischemia.…”

Section: Anti-inflammatory Effects Of Pyruvatementioning

confidence: 99%

Pyruvate enhances neurological recovery following cardiopulmonary arrest and resuscitation

et al. 2008

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Purpose-Cerebral oxidative stress and metabolic dysfunction impede neurological recovery from cardiac arrest-resuscitation. Pyruvate, a potent antioxidant and energy-yielding fuel, has been shown to protect against oxidant-and ischemia-induced neuronal damage. This study tested whether acute pyruvate treatment during cardiopulmonary resuscitation can prevent neurological dysfunction and cerebral injury following cardiac arrest. Methods-Anesthetized, open-chest mongrel dogs underwent 5 min cardiac arrest, 5 min open chest cardiac compression (OCCC), defibrillation and 3 day recovery. Pyruvate (n = 9) or NaCl volume control (n = 8) were administered (0.125 mmol/kg/min iv) throughout OCCC and the first 55 min recovery. Sham dogs (n = 6) underwent surgery and recovery without cardiac arrestresuscitation.Results-Neurological deficit score (NDS), evaluated at 2 day recovery, was sharply increased in NaCl-treated dogs (10.3 ± 3.5) vs. shams (1.2 ± 0.4), but pyruvate treatment mitigated neurological deficit (NDS = 3.3 ± 1.2; P < 0.05 vs. NaCl). Brain samples were taken for histological examination and evaluation of inflammation and cell death at 3 d recovery. Loss of pyramidal neurons in the hippocampal CA1 subregion was greater in the NaCl controls than in pyruvate treated dogs (11.7 ± 2.3% vs. 4.3 ± 1.2%; P < 0.05). Cardiac arrest increased caspase 3 activity, matrix metalloproteinase activity, and DNA fragmentation in the CA1 subregion; pyruvate prevented caspase-3 activation and DNA fragmentation, and suppressed matrix metalloproteinase activity.Conclusion-Intravenous pyruvate therapy during cardiopulmonary resuscitation prevents initial oxidative stress and neuronal injury and enhances neurological recovery from cardiac arrest.

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Section: Anti-inflammatory Effects Of Pyruvatementioning

confidence: 99%

Pyruvate enhances neurological recovery following cardiopulmonary arrest and resuscitation

et al. 2008

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“…[4][5][6][7][8] Unlike more commonly used stroke models, use of this model for investigating cerebral edema or necrosis has been reported by only a few laboratories. 9,10 Detection of apoptosis in living subjects using advanced diffusion-weighted imaging (DWI) is difficult because the process is not associated with either abnormal water content or gross morphologic changes. However, recent advances in ligand-targeting contrast agents have shown that it is possible to detect the process of cellular apoptosis in vivo.…”

mentioning

confidence: 99%

“…4–8 Unlike more commonly used stroke models, use of this model for investigating cerebral edema or necrosis has been reported by only a few laboratories. 9,10…”

mentioning

confidence: 99%

Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain

Liu

Huang²,

Kim³

et al. 2007

Mol Imaging

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Brain injury affects one-third of persons who survive after heart attack, even with restoration of spontaneous circulation by cardiopulmonary resuscitation. We studied brain injury resulting from transient bilateral carotid artery occlusion (BCAO) and reperfusion by simulating heart attack and restoration of circulation, respectively, in live C57Black6 mice. This model is known to induce neuronal death in the hippocampus, striatum, and cortex. We report the appearance of edema after transient BCAO of 60 minutes and 1 day of reperfusion. Hyperintensity in diffusion-weighted magnetic resonance imaging (MRI) was detectable in the striatum, thalamus, and cortex but not in the hippocampus. To determine whether damage to the hippocampus can be detected in live animals, we infused a T(2) susceptibility magnetic resonance contrast agent (superparamagnetic iron oxide nanoparticles [SPIONs]) that was linked to single-stranded deoxyribonucleic acid (DNA) complementary in sequence to c-fos messenger ribonucleic acid (SPION-cfos); we acquired in vivo T(2)*-weighted MRI 3 days later. SPION retention was measured as T(2)* (milliseconds) signal reduction or R(2)* value (s(-1)) elevation. We found that animals treated with 60-minute BCAO and 7-day reperfusion exhibited significantly less SPION retention in the hippocampus and cortex than sham-operated animals. These findings suggest that brain injury induced by cardiac arrest can be detected in live animals.

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Cerebral Edema After Cardiopulmonary Resuscitation: A Therapeutic Target Following Cardiac Arrest?

et al. 2017

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We sought to review the role that cerebral edema plays in neurologic outcome following cardiac arrest, to understand whether cerebral edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, cerebral edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. Like other conditions characterized by cerebral ischemia/reperfusion, neuroprotection after cardiac arrest has proven to be difficult to achieve. Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood-brain barrier. Limited preclinical data suggest that strategies to reduce cerebral edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting cerebral edema will improve patient outcomes after cardiac arrest.

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Matrix metalloproteinases are not involved in early brain edema formation after cardiac arrest in rats

Cited by 3 publications

References 33 publications

Pyruvate enhances neurological recovery following cardiopulmonary arrest and resuscitation

Pyruvate enhances neurological recovery following cardiopulmonary arrest and resuscitation

Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain

Cerebral Edema After Cardiopulmonary Resuscitation: A Therapeutic Target Following Cardiac Arrest?

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