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Brain Sciences
Special Issues
Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke
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Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke

A special issue of Brain Sciences (ISSN 2076-3425).

Deadline for manuscript submissions: closed (28 February 2018) | Viewed by 36807

Special Issue Editor

Prof. Dr. Bruno Meloni

E-Mail Website
Guest Editor
1. Stroke Research Group/Head of Laboratory Research, Perron Institute for Neurological and Translational Sciences, Nedlands, WA 6009, Australia
2. Centre for Neuromuscular and Neurological Disorders, The University of Western Australia, Nedlands, WA 6009, Australia
3. Department of Neurosurgery, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia
Interests: neuroprotection; stroke; hypoxic-ischaemic encephalopathy; traumatic brain injury; in vitro neuronal cell injury models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hypoxic-ischemic brain injury and stroke are devastating conditions which can affect individuals at any age from birth to old age. Acute brain injury resulting from stroke and hypoxic-ischaemic (HI) episodes, including perinatal HI encephalopathy (HIE) and global cerebral ischemia together, are one of the major causes of death and disability worldwide. Despite considerable research over many years, there are still no clinically effective pharmacological neuroprotective treatments capable of reducing the severity of brain injury in these situations. As a consequence, the development of an effective pharmacological neuroprotective agent for individuals suffering a stroke or a hypoxic-ischemic event remains an urgent unmet need.

Furthermore, many of the pathophysiological events associated with ischaemic and hypoxic brain injury have not been fully elucidated and therefore further studies are required in this area. Ultimately, a better understanding of the pathophysiology of ischaemic and hypoxic brain injury will aid the develeopment of new and effective neuroprotective therapies. Hence, the aim of this Special Issue is to encourage the publication of new experimental and clinical findings to advance our understanding of the pathogenic processes and the development of neuroprotective strategies following hypoxic-ischemic brain injury and stroke.

Prof. Bruno Meloni
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

  • Stroke
  • Hypoxic-ischemic brain injury
  • Global cerebral ischemia
  • Perinatal hypoxic-ischemic encephalopathy
  • Neuronal death
  • Neuroprotection
  • Pathophysiology

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Published Papers (6 papers)

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Editorial

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177 KiB  
Editorial
Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke
by Bruno P. Meloni
Brain Sci. 2017, 7(8), 110; https://doi.org/10.3390/brainsci7080110 - 22 Aug 2017
Cited by 10 | Viewed by 5218
Abstract
Hypoxic-ischemic brain injury and stroke are closely related and devastating conditions that can affect individuals of all ages.[...] Full article
(This article belongs to the Special Issue Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke)

Research

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11 pages, 2824 KiB  
Article
Pretreatment with Group II Metabotropic Glutamate Receptor Agonist LY379268 Protects Neonatal Rat Brains from Oxidative Stress in an Experimental Model of Birth Asphyxia
by Ewelina Bratek, Apolonia Ziembowicz and Elzbieta Salinska
Brain Sci. 2018, 8(3), 48; https://doi.org/10.3390/brainsci8030048 - 17 Mar 2018
Cited by 12 | Viewed by 4900
Abstract
Hypoxia-ischemia (H-I) at the time of birth may cause neonatal death or lead to persistent brain damage. The search for an effective treatment of asphyxiated infants has not resulted in an effective therapy, and hypothermia remains the only available therapeutic strategy. Among possible [...] Read more.
Hypoxia-ischemia (H-I) at the time of birth may cause neonatal death or lead to persistent brain damage. The search for an effective treatment of asphyxiated infants has not resulted in an effective therapy, and hypothermia remains the only available therapeutic strategy. Among possible experimental therapies, the induction of ischemic tolerance is promising. Recent investigations have shown that activation of group II metabotropic glutamate receptors (mGluR2/3) can provide neuroprotection against H-I, but the mechanism of this effect is not clear. The aim of this study was to investigate whether an mGluR2/3 agonist applied before H-I reduces brain damage in an experimental model of birth asphyxia and whether a decrease in oxidative stress plays a role in neuroprotection. Neonatal H-I on seven-day-old rats was used as an experimental model of birth asphyxia. Rats were injected intraperitoneally with the mGluR2/3 agonist LY379268 24 or 1 h before H-I (5 mg/kg). LY379268 reduced the infarct area in the ischemic hemisphere. Application of the agonist at both times also reduced the elevated levels of reactive oxygen species (ROS) in the ipsilateral hemisphere observed after H-I and prevented the increase in antioxidant enzyme activity in the injured hemisphere. The decrease in glutathione (GSH) level was also restored after agonist application. The results suggest that the neuroprotective mechanisms triggered by the activation of mGluR2/3 before H-I act through the decrease of glutamate release and its extracellular concentration resulting in the inhibition of ROS production and reduction of oxidative stress. This, rather than induction of ischemic tolerance, is probably the main mechanism involved in the observed neuroprotection. Full article
(This article belongs to the Special Issue Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke)
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18 pages, 2148 KiB  
Article
Abstraction and Idealization in Biomedicine: The Nonautonomous Theory of Acute Cell Injury
by Donald J. DeGracia, Doaa Taha, Fika Tri Anggraini, Shreya Sutariya, Gabriel Rababeh and Zhi-Feng Huang
Brain Sci. 2018, 8(3), 39; https://doi.org/10.3390/brainsci8030039 - 27 Feb 2018
Cited by 1 | Viewed by 4214
Abstract
Neuroprotection seeks to halt cell death after brain ischemia and has been shown to be possible in laboratory studies. However, neuroprotection has not been successfully translated into clinical practice, despite voluminous research and controlled clinical trials. We suggested these failures may be due, [...] Read more.
Neuroprotection seeks to halt cell death after brain ischemia and has been shown to be possible in laboratory studies. However, neuroprotection has not been successfully translated into clinical practice, despite voluminous research and controlled clinical trials. We suggested these failures may be due, at least in part, to the lack of a general theory of cell injury to guide research into specific injuries. The nonlinear dynamical theory of acute cell injury was introduced to ameliorate this situation. Here we present a revised nonautonomous nonlinear theory of acute cell injury and show how to interpret its solutions in terms of acute biomedical injuries. The theory solutions demonstrate the complexity of possible outcomes following an idealized acute injury and indicate that a “one size fits all” therapy is unlikely to be successful. This conclusion is offset by the fact that the theory can (1) determine if a cell has the possibility to survive given a specific acute injury, and (2) calculate the degree of therapy needed to cause survival. To appreciate these conclusions, it is necessary to idealize and abstract complex physical systems to identify the fundamental mechanism governing the injury dynamics. The path of abstraction and idealization in biomedical research opens the possibility for medical treatments that may achieve engineering levels of precision. Full article
(This article belongs to the Special Issue Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke)
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3185 KiB  
Article
Integrity of Cerebellar Fastigial Nucleus Intrinsic Neurons Is Critical for the Global Ischemic Preconditioning
by Eugene V. Golanov, Angelique S. Regnier-Golanov and Gavin W. Britz
Brain Sci. 2017, 7(10), 121; https://doi.org/10.3390/brainsci7100121 - 21 Sep 2017
Cited by 8 | Viewed by 6573
Abstract
Excitation of intrinsic neurons of cerebellar fastigial nucleus (FN) renders brain tolerant to local and global ischemia. This effect reaches a maximum 72 h after the stimulation and lasts over 10 days. Comparable neuroprotection is observed following sublethal global brain ischemia, a phenomenon [...] Read more.
Excitation of intrinsic neurons of cerebellar fastigial nucleus (FN) renders brain tolerant to local and global ischemia. This effect reaches a maximum 72 h after the stimulation and lasts over 10 days. Comparable neuroprotection is observed following sublethal global brain ischemia, a phenomenon known as preconditioning. We hypothesized that FN may participate in the mechanisms of ischemic preconditioning as a part of the intrinsic neuroprotective mechanism. To explore potential significance of FN neurons in brain ischemic tolerance we lesioned intrinsic FN neurons with excitotoxin ibotenic acid five days before exposure to 20 min four-vessel occlusion (4-VO) global ischemia while analyzing neuronal damage in Cornu Ammoni area 1 (CA1) hippocampal area one week later. In FN-lesioned animals, loss of CA1 cells was higher by 22% compared to control (phosphate buffered saline (PBS)-injected) animals. Moreover, lesion of FN neurons increased morbidity following global ischemia by 50%. Ablation of FN neurons also reversed salvaging effects of five-minute ischemic preconditioning on CA1 neurons and morbidity, while ablation of cerebellar dentate nucleus neurons did not change effect of ischemic preconditioning. We conclude that FN is an important part of intrinsic neuroprotective system, which participates in ischemic preconditioning and may participate in naturally occurring neuroprotection, such as “diving response”. Full article
(This article belongs to the Special Issue Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke)
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Review

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31 pages, 748 KiB  
Review
Neuroprotective Effects of Bioactive Compounds and MAPK Pathway Modulation in “Ischemia”—Stressed PC12 Pheochromocytoma Cells
by Adi Lahiani, Annette Brand-Yavin, Ephraim Yavin and Philip Lazarovici
Brain Sci. 2018, 8(2), 32; https://doi.org/10.3390/brainsci8020032 - 8 Feb 2018
Cited by 32 | Viewed by 7775
Abstract
This review surveys the efforts taken to investigate in vitro neuroprotective features of synthetic compounds and cell-released growth factors on PC12 clonal cell line temporarily deprived of oxygen and glucose followed by reoxygenation (OGD/R). These cells have been used previously to mimic some [...] Read more.
This review surveys the efforts taken to investigate in vitro neuroprotective features of synthetic compounds and cell-released growth factors on PC12 clonal cell line temporarily deprived of oxygen and glucose followed by reoxygenation (OGD/R). These cells have been used previously to mimic some of the properties of in vivo brain ischemia-reperfusion-injury (IRI) and have been instrumental in identifying common mechanisms such as calcium overload, redox potential, lipid peroxidation and MAPKs modulation. In addition, they were useful for establishing the role of certain membrane penetrable cocktails of antioxidants as well as potential growth factors which may act in neuroprotection. Pharmacological mechanisms of neuroprotection addressing modulation of the MAPK cascade and increased redox potential by natural products, drugs and growth factors secreted by stem cells, in either undifferentiated or nerve growth factor-differentiated PC12 cells exposed to ischemic conditions are discussed for future prospects in neuroprotection studies. Full article
(This article belongs to the Special Issue Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke)
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Other

8 pages, 878 KiB  
Case Report
Recurrent Hemorrhagic Conversion of Ischemic Stroke in a Patient with Mechanical Heart Valve: A Case Report and Literature Review
by Micheal Jace Tarver, Tyler Schmidt and Michael T. Koltz
Brain Sci. 2018, 8(1), 12; https://doi.org/10.3390/brainsci8010012 - 7 Jan 2018
Cited by 1 | Viewed by 6733
Abstract
The authors present a unique case of recurrent stroke, discovered to be secondary to hemorrhagic conversion of microemboli from a mechanical aortic valve despite anticoagulation with Coumadin. The complexity of this case was magnified by the patient’s young age, a mechanical heart valve [...] Read more.
The authors present a unique case of recurrent stroke, discovered to be secondary to hemorrhagic conversion of microemboli from a mechanical aortic valve despite anticoagulation with Coumadin. The complexity of this case was magnified by the patient’s young age, a mechanical heart valve (MHV), and a need for anticoagulation to maintain MHV patency in a setting of potentially life-threatening intracranial hemorrhage. Anticoagulant and antiplatelet therapy are risk factors for hemorrhagic conversion post-cerebral ischemia; however, the pathophysiology underlying endothelial cell dysfunction causing red blood cell extravasation is an active area of basic and clinical research. The need for randomized clinical trials to aid in the creation of standardized treatment protocol continues to go unmet. Consequently, there is marked variation in therapeutic approaches to treating intracranial hemorrhage in patients with an MHV. Unfortunately, patients with an MHV are considered at high thromboembolic (TE) risk, and these patients are often excluded from clinical trials of acute stroke due to their increased TE potential. The authors feel this case represents an example of endothelial dysfunction secondary to microthrombotic events originating from an MHV, which caused ischemic stroke with hemorrhagic conversion complicated by the need for anticoagulation for an MHV. This case offers a definitive treatment algorithm for a complex clinical dilemma. Full article
(This article belongs to the Special Issue Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke)
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