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  1. Article ; Online: The splenic response to stroke: from rodents to stroke subjects.

    Seifert, Hilary A / Offner, Halina

    Journal of neuroinflammation

    2018  Volume 15, Issue 1, Page(s) 195

    Abstract: Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in ... ...

    Abstract Background: Stroke is the fifth leading cause of death and the leading cause of long-term disability in the USA, costing $40.2 billion in direct and indirect costs. Globally, stroke is the second leading cause of death and has a higher prevalence in lower- and middle-income countries compared to high-income countries. The role of the spleen in stroke has been studied in rodent models of stroke and is seen as a major contributor to increased secondary neural injury after stroke. Splenectomy 2 weeks prior to ischemic and hemorrhagic stroke in mice and rats shows decreased infarct volumes. Additionally, the spleen decreases in size following stroke in rodents. Pro-inflammatory mediators are also increased in the spleen and subsequently the brain after stroke. These data in preclinical models of stroke have led stroke neurologists to look at the splenic response in stroke subjects. The outcomes of these studies suggest the spleen is responding in a similar manner in stroke subjects as it is in animal models of stroke.
    Conclusion: Animal models demonstrating the detrimental role of the spleen in stroke are providing strong evidence of how the spleen is responding during stroke in human subjects. This indicates treatments targeting the splenic immune response in animals could provide useful targets and treatments for stroke subjects.
    MeSH term(s) Animals ; Disease Models, Animal ; Humans ; Mice ; Rats ; Spleen/physiology ; Splenectomy ; Stroke/immunology ; Stroke/pathology
    Language English
    Publishing date 2018-07-03
    Publishing country England
    Document type Journal Article ; Review
    ISSN 1742-2094
    ISSN (online) 1742-2094
    DOI 10.1186/s12974-018-1239-9
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  2. Article ; Online: Regulatory B cells in experimental stroke.

    Seifert, Hilary A / Vandenbark, Arthur A / Offner, Halina

    Immunology

    2018  Volume 154, Issue 2, Page(s) 169–177

    Abstract: Current treatment options for human stroke are limited mainly to the modestly effective infusion of tissue plasminogen activator (tPA), with additional improvement of functional independence and higher rates of angiographic revascularization observed ... ...

    Abstract Current treatment options for human stroke are limited mainly to the modestly effective infusion of tissue plasminogen activator (tPA), with additional improvement of functional independence and higher rates of angiographic revascularization observed after mechanical thrombectomy. However, new therapeutic strategies that address post-stroke immune-mediated inflammatory responses are urgently needed. Recent studies in experimental stroke have firmly implicated immune mechanisms in the propagation and partial resolution of central nervous system damage after the ischaemic event. A new-found anti-inflammatory role for regulatory B (Breg) cells in autoimmune diseases sparked interest in these cells as potential immunomodulators in stroke. Subsequent studies identified interleukin-10 as a common regulatory cytokine among all five of the currently recognized Breg cell subsets, several of which can be found in the affected brain hemisphere after induction of experimental stroke in mice. Transfer of enriched Breg cell subpopulations into both B-cell-depleted and wild-type mice confirmed their potent immunosuppressive activities in vivo, including recruitment and potentiation of regulatory T cells. Moreover, Breg cell therapy strongly reduced stroke volumes and treatment outcomes in ischaemic mice even when administered 24 hr after induction of experimental stroke, a treatment window far exceeding that of tPA. These striking results suggest that transfer of enriched Breg cell populations could have therapeutic value in human stroke, although considerable clinical challenges remain.
    MeSH term(s) Animals ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; B-Lymphocyte Subsets/immunology ; B-Lymphocyte Subsets/metabolism ; B-Lymphocytes, Regulatory/immunology ; B-Lymphocytes, Regulatory/metabolism ; Cell Communication/immunology ; Cytokines/metabolism ; Disease Models, Animal ; Disease Susceptibility/immunology ; Humans ; Stroke/etiology ; Stroke/metabolism ; Stroke/pathology
    Chemical Substances Cytokines
    Language English
    Publishing date 2018-02-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.12887
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  3. Article ; Online: Molecular and cellular immune responses to ischemic brain injury.

    Seifert, Hilary A / Pennypacker, Keith R

    Translational stroke research

    2014  Volume 5, Issue 5, Page(s) 543–553

    Abstract: Despite extensive research into stroke pathology, there have not been any major recent advancements in stroke therapeutics. Animal models of cerebral ischemia and clinical data have been used to investigate the progressive neural injury that occurs after ...

    Abstract Despite extensive research into stroke pathology, there have not been any major recent advancements in stroke therapeutics. Animal models of cerebral ischemia and clinical data have been used to investigate the progressive neural injury that occurs after an initial ischemic insult. This has lead researchers to focus more on the peripheral immune response that is generated as a result of cerebral ischemia. The therapies that have been developed as a result of this research thus far have proven ineffective in clinical trials. The failure of these therapeutics in clinical trials is thought to be due to the broad immunosuppression elicited as a result of the treatments and the cerebral ischemia itself. Emerging evidence indicates a more selective modulation of the immune system following stroke could be beneficial. The spleen has been shown to exacerbate neural injury following experimental stroke and would provide a strong therapeutic target. Selecting facets of the immune system to target would allow the protective and regenerative properties of the immune response to remain intact while blunting the pro-inflammatory response generated towards the injured brain.
    MeSH term(s) Animals ; Brain/immunology ; Brain Ischemia/immunology ; Brain Ischemia/therapy ; Cytokines/immunology ; Disease Models, Animal ; Humans ; Immunity, Cellular ; Spleen/immunology ; Stem Cell Transplantation ; Stroke/immunology ; Stroke/therapy ; T-Lymphocytes/immunology
    Chemical Substances Cytokines
    Language English
    Publishing date 2014-06-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2541897-X
    ISSN 1868-601X ; 1868-4483
    ISSN (online) 1868-601X
    ISSN 1868-4483
    DOI 10.1007/s12975-014-0349-7
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  4. Article ; Online: Estrogen-induced compensatory mechanisms protect IL-10-deficient mice from developing EAE.

    Seifert, Hilary A / Gerstner, Grant / Kent, Gail / Vandenbark, Arthur A / Offner, Halina

    Journal of neuroinflammation

    2019  Volume 16, Issue 1, Page(s) 195

    Abstract: Background: IL-10 knockout (KO) mice are protected from experimental autoimmune encephalomyelitis (EAE) with low-dose estrogen (E2) treatment similar to wild-type (WT) mice. Previous studies have demonstrated a decrease in tumor necrosis factor in all ... ...

    Abstract Background: IL-10 knockout (KO) mice are protected from experimental autoimmune encephalomyelitis (EAE) with low-dose estrogen (E2) treatment similar to wild-type (WT) mice. Previous studies have demonstrated a decrease in tumor necrosis factor in all E2-treated groups, which led to the protection of the mice.
    Methods: This study used IL-10 KO mice and WT mice treated either with E2 or sham pellets 7 days prior to induction of EAE. Mice were observed for 21 days post-immunization. The spleen, inguinal lymph nodes, and brain were evaluated by flow cytometry. Spinal cords were evaluated using a cytokine/chemokine array, RT-PCR, and histology.
    Results: This study demonstrates that E2 treatment induced three heightened regulatory mechanisms that potentially protect IL-10 KO mice from EAE: (1) an increase in programmed death-ligands 1 and 2 on monocytes and macrophages in the periphery and within the CNS; (2) an increase in CD73 in the inflamed CNS, which can increase the production of the anti-inflammatory molecule adenosine; and (3) a decrease in CD4
    Conclusion: These results indicate that previously unrecognized compensatory mechanisms of EAE protection are stimulated by E2 in the absence of IL-10, which can provide disease protection comparable to the IL-10-dependent effects induced by E2 in WT mice.
    MeSH term(s) Animals ; Drug Implants/administration & dosage ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/prevention & control ; Estrogens/administration & dosage ; Female ; Interleukin-10/deficiency ; Mice ; Mice, Inbred C57BL ; Mice, Knockout
    Chemical Substances Drug Implants ; Estrogens ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2019-10-29
    Publishing country England
    Document type Journal Article
    ISSN 1742-2094
    ISSN (online) 1742-2094
    DOI 10.1186/s12974-019-1588-z
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  5. Article ; Online: Sex differences in the therapeutic effects of anti-PDL2 neutralizing antibody on stroke.

    Seifert, Hilary A / Zhu, Wenbin / Vandenbark, Arthur A / Alkayed, Nabil J / Offner, Halina

    Metabolic brain disease

    2019  Volume 34, Issue 6, Page(s) 1705–1712

    Abstract: Inflammation involving migration of immune cells across the damaged blood-brain barrier (BBB), activation of resident innate microglia and production of inflammatory humoral mediators such as cytokines and chemokines play a critical role in the ... ...

    Abstract Inflammation involving migration of immune cells across the damaged blood-brain barrier (BBB), activation of resident innate microglia and production of inflammatory humoral mediators such as cytokines and chemokines play a critical role in the pathogenesis of ischemic stroke. Cell-cell signaling involved in the process also includes checkpoint interaction between programmed death receptor (PD1) and programmed death ligands, PDL1 and PDL2. Based on our previous studies showing reduced MCAO infarct volumes in PDL2 deficient mice, we evaluated the ability of anti-PDL2 mAb to treat MCAO in male and female C57BL/6 mice. We found that anti-PDL2 neutralizing antibody treatment of MCAO significantly reduced infarct volumes in male mice but had no protective effects in female mice even at a 5-fold increased dose of anti-PDL2 mAb. The protection in male mice was likely mediated by reduced percentages in the spleen of PDL2
    MeSH term(s) Animals ; Antibodies, Neutralizing/therapeutic use ; Disease Models, Animal ; Female ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/immunology ; Male ; Mice ; Programmed Cell Death 1 Ligand 2 Protein/immunology ; Sex Factors ; Stroke/drug therapy ; Stroke/immunology ; T-Lymphocyte Subsets/immunology ; Treatment Outcome
    Chemical Substances Antibodies, Neutralizing ; Pdcd1lg2 protein, mouse ; Programmed Cell Death 1 Ligand 2 Protein
    Language English
    Publishing date 2019-08-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 632824-6
    ISSN 1573-7365 ; 0885-7490
    ISSN (online) 1573-7365
    ISSN 0885-7490
    DOI 10.1007/s11011-019-00476-3
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  6. Article ; Online: Estrogen protects both sexes against EAE by promoting common regulatory cell subtypes independent of endogenous estrogen.

    Seifert, Hilary A / Benedek, Gil / Nguyen, Ha / Kent, Gail / Vandenbark, Arthur A / Offner, Halina

    Metabolic brain disease

    2017  Volume 32, Issue 5, Page(s) 1747–1754

    Abstract: Autoimmune diseases including multiple sclerosis predominantly affect females. Although high levels of sex hormones, particularly estrogen (E2), can reduce proinflammatory immune responses, it remains unclear if a lack of endogenous sex hormones might ... ...

    Abstract Autoimmune diseases including multiple sclerosis predominantly affect females. Although high levels of sex hormones, particularly estrogen (E2), can reduce proinflammatory immune responses, it remains unclear if a lack of endogenous sex hormones might affect treatment with exogenous sex hormones. Pretreatment with E2 almost completely prevents intact female and male mice from developing clinical and histological signs of experimental autoimmune encephalomyelitis (EAE) by promoting various regulatory immune cell phenotypes. To evaluate the effects of exogenous estrogen in the absence of endogenous sex hormones, the current study compared EAE severity and the emergence of different immunoregulatory cell populations after E2 pretreatment of ovariectomized (OVX) female versus male mice. We found that E2 equally protected both OVX females and males from EAE over a 21 day observation period concomitant with reduced total cell numbers in spleen and spinal cord (males only), but enhanced percentages of CD19
    MeSH term(s) Animals ; Antigens, CD/metabolism ; B-Lymphocytes, Regulatory/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Encephalomyelitis, Autoimmune, Experimental/prevention & control ; Estradiol/metabolism ; Estradiol/therapeutic use ; Female ; Macrophages/drug effects ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Ovariectomy ; Spinal Cord/pathology ; Spleen/pathology ; T-Lymphocytes, Regulatory
    Chemical Substances Antigens, CD ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2017-07-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 632824-6
    ISSN 1573-7365 ; 0885-7490
    ISSN (online) 1573-7365
    ISSN 0885-7490
    DOI 10.1007/s11011-017-0063-8
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  7. Article ; Online: Antibiotics protect against EAE by increasing regulatory and anti-inflammatory cells.

    Seifert, Hilary A / Benedek, Gil / Nguyen, Ha / Gerstner, Grant / Zhang, Ying / Kent, Gail / Vandenbark, Arthur A / Bernhagen, Jürgen / Offner, Halina

    Metabolic brain disease

    2018  Volume 33, Issue 5, Page(s) 1599–1607

    Abstract: A seven day pretreatment course of an oral antibiotic cocktail (Ampicillin, Metronidazole, Neomycin Sulfate, and Vancomycin) was shown to induce changes in peripheral immune regulation and protect mice from signs of experimental autoimmune ... ...

    Abstract A seven day pretreatment course of an oral antibiotic cocktail (Ampicillin, Metronidazole, Neomycin Sulfate, and Vancomycin) was shown to induce changes in peripheral immune regulation and protect mice from signs of experimental autoimmune encephalomyelitis (EAE). To determine if a shorter course of antibiotic pretreatment could also protect the mice from EAE and induce regulatory immune cells, studies were conducted using the same oral antibiotic cocktail for three days. In addition, the CNS was examined to determine the effects of antibiotic pretreatment on EAE disease course and immune modulation within the affected tissue. The shorter three day pretreatment course was also significantly protective against severe EAE in C57BL/6 mice. Moreover, our study found increased frequencies of regulatory cells and a decrease in the frequency of anti-inflammatory macrophages in the spleen of EAE protected mice. Additionally, a chemokine and chemokine receptor array run on mRNA from spinal cords revealed that genes associated with regulatory T cells and macrophage recruitment were strongly upregulated in the antibiotic pretreated mice. Additional RT-PCR data showed genes associated with anti-inflammatory microglia/macrophages were upregulated and pro-inflammatory genes were downregulated. This suggests the macrophages recruited to the spinal cord by chemokines are subsequently polarized toward an anti-inflammatory phenotype. These results lend strong support to the conclusion that a three day course of antibiotic treatment given prior to the induction of severe EAE profoundly protected the mice by inducing regulatory lymphocytes in the periphery and an anti-inflammatory milieu in the affected spinal cord tissue.
    MeSH term(s) Animals ; Anti-Bacterial Agents/administration & dosage ; Anti-Bacterial Agents/pharmacology ; B-Lymphocytes/drug effects ; B-Lymphocytes/metabolism ; Chemokines/genetics ; Down-Regulation/genetics ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/prevention & control ; Female ; Immunomodulation ; Lymph Nodes/cytology ; Lymph Nodes/drug effects ; Macrophages/drug effects ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Microglia/drug effects ; Microglia/immunology ; Receptors, Chemokine/genetics ; Spinal Cord/drug effects ; Spinal Cord/physiopathology ; Spleen/drug effects ; Spleen/immunology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Up-Regulation/genetics
    Chemical Substances Anti-Bacterial Agents ; Chemokines ; Receptors, Chemokine
    Language English
    Publishing date 2018-06-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 632824-6
    ISSN 1573-7365 ; 0885-7490
    ISSN (online) 1573-7365
    ISSN 0885-7490
    DOI 10.1007/s11011-018-0266-7
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  8. Article ; Online: Sex differences in regulatory cells in experimental stroke.

    Seifert, Hilary A / Benedek, Gil / Liang, Jian / Nguyen, Ha / Kent, Gail / Vandenbark, Arthur A / Saugstad, Julie A / Offner, Halina

    Cellular immunology

    2017  Volume 318, Page(s) 49–54

    Abstract: Stroke is the leading cause of disability in the United States. Sex differences, including smaller infarcts in females and greater involvement of immune-mediated inflammation in males may affect the efficacy of immune-modulating interventions. To address ...

    Abstract Stroke is the leading cause of disability in the United States. Sex differences, including smaller infarcts in females and greater involvement of immune-mediated inflammation in males may affect the efficacy of immune-modulating interventions. To address these differences, we sought to identify distinct stroke-modifying mechanisms in female vs. male mice. The current study demonstrated smaller infarcts and increased levels of regulatory CD19
    MeSH term(s) Animals ; B-Lymphocytes, Regulatory/immunology ; Brain/immunology ; Brain/pathology ; Cells, Cultured ; Disease Models, Animal ; Female ; Humans ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Middle Cerebral Artery/surgery ; Sex ; Sex Factors ; Stroke/immunology
    Language English
    Publishing date 2017-06-08
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80094-6
    ISSN 1090-2163 ; 0008-8749
    ISSN (online) 1090-2163
    ISSN 0008-8749
    DOI 10.1016/j.cellimm.2017.06.003
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    Zs.A 417: Show issues Location:
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  9. Article ; Online: Leukemia Inhibitory Factor Protects Neurons from Ischemic Damage via Upregulation of Superoxide Dismutase 3.

    Davis, Stephanie M / Collier, Lisa A / Leonardo, Christopher C / Seifert, Hilary A / Ajmo, Craig T / Pennypacker, Keith R

    Molecular neurobiology

    2016  Volume 54, Issue 1, Page(s) 608–622

    Abstract: Leukemia inhibitory factor (LIF) has been shown to protect oligodendrocytes from ischemia by upregulating endogenous antioxidants. The goal of this study was to determine whether LIF protects neurons during stroke by upregulating superoxide dismutase 3 ( ... ...

    Abstract Leukemia inhibitory factor (LIF) has been shown to protect oligodendrocytes from ischemia by upregulating endogenous antioxidants. The goal of this study was to determine whether LIF protects neurons during stroke by upregulating superoxide dismutase 3 (SOD3). Animals were administered phosphate-buffered saline (PBS) or 125 μg/kg LIF at 6, 24, and 48 h after middle cerebral artery occlusion or sham surgery. Neurons were isolated from rat pups on embryonic day 18 and used between 7 and 15 days in culture. Cells were treated with LIF and/or 10 μM Akt inhibitor IV with PBS and 0.1 % DMSO acting as vehicle controls. Neurons transfected with scrambled or SOD3 small interfering RNA (siRNA) were subjected to 24-h ischemia after PBS or LIF treatment. LIF significantly increased superoxide dismutase activity and SOD3 expression in ipsilateral brain tissue compared to PBS. Following 24-h ischemia, LIF reduced cell death and increased SOD3 messenger RNA (mRNA) in vitro compared to PBS. Adding Akt inhibitor IV with LIF counteracted the decrease in cell death. Partially silencing the expression of SOD3 using siRNA prior to LIF treatment counteracted the protective effect of LIF-alone PBS treatment. These results indicate that LIF protects neurons in vivo and in vitro via upregulation of SOD3.
    MeSH term(s) Animals ; Cell Hypoxia/drug effects ; Cell Hypoxia/physiology ; Cells, Cultured ; Cerebral Cortex/drug effects ; Cerebral Cortex/enzymology ; Cerebral Cortex/pathology ; Dose-Response Relationship, Drug ; Leukemia Inhibitory Factor/pharmacology ; Male ; Neurons/drug effects ; Neurons/enzymology ; Neurons/pathology ; Neuroprotective Agents/pharmacology ; Rats ; Superoxide Dismutase/biosynthesis ; Up-Regulation/drug effects ; Up-Regulation/physiology
    Chemical Substances LIF protein, human ; Leukemia Inhibitory Factor ; Neuroprotective Agents ; Sod3 protein, rat (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1)
    Language English
    Publishing date 2016-01-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-015-9587-2
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    Zs.A 2411: Show issues Location:
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  10. Article ; Online: Translational Evaluation of Acid/Base and Electrolyte Alterations in Rodent Model of Focal Ischemia.

    Martha, Sarah R / Collier, Lisa A / Davis, Stephanie M / Seifert, Hilary A / Leonardo, Christopher C / Ajmo, Craig T / Foran, Elspeth A / Fraser, Justin F / Pennypacker, Keith R

    Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association

    2018  Volume 27, Issue 10, Page(s) 2746–2754

    Abstract: Background and purpose: Acid/base and electrolytes could provide clinically valuable information about cerebral infarct core and penumbra. We evaluated associations between acid/base and electrolyte changes and outcomes in 2 rat models of stroke, ... ...

    Abstract Background and purpose: Acid/base and electrolytes could provide clinically valuable information about cerebral infarct core and penumbra. We evaluated associations between acid/base and electrolyte changes and outcomes in 2 rat models of stroke, permanent, and transient middle cerebral artery occlusion.
    Methods: Three-month old Sprague-Dawley rats underwent permanent or transient middle cerebral artery occlusion. Pre- and post-middle cerebral artery occlusion venous samples for permanent and transient models provided pH, carbon dioxide, oxygen, glucose, and electrolyte values of ionized calcium, potassium, and sodium. Multiple regression determined predictors of infarct volume from these values, and Kaplan-Meier curve analyzed morality between permanent and transient middle cerebral artery occlusion models.
    Results: Analysis indicated significant differences in the blood gas and electrolytes between pre- to post-middle cerebral artery occlusion. A decrease in pH and sodium with increases in carbon dioxide, potassium, ionized calcium, and glucose changes were found in both middle cerebral artery occlusion models; while hematocrit and hemoglobin were significant in the transient model. pH and ionized calcium were predictors of infarct volume in the permanent model, as changes in pH and ionized calcium decreased, infarct volume increased.
    Conclusions: There are acute changes in acid/base balance and electrolytes during stroke in transient and permanent rodent models. Additionally, we found pH and ionized calcium changes predicted stroke volume in the permanent middle cerebral artery occlusion model. These preliminary findings are novel, and warrant further exploration in human conditions.
    MeSH term(s) Acid-Base Equilibrium ; Animals ; Biomarkers/blood ; Blood Glucose/metabolism ; Calcium/blood ; Carbon Dioxide/blood ; Disease Models, Animal ; Hemoglobins/metabolism ; Hydrogen-Ion Concentration ; Infarction, Middle Cerebral Artery/blood ; Infarction, Middle Cerebral Artery/pathology ; Infarction, Middle Cerebral Artery/physiopathology ; Oxygen/blood ; Potassium/blood ; Rats, Sprague-Dawley ; Sodium/blood ; Time Factors ; Water-Electrolyte Balance
    Chemical Substances Biomarkers ; Blood Glucose ; Hemoglobins ; Carbon Dioxide (142M471B3J) ; Sodium (9NEZ333N27) ; Potassium (RWP5GA015D) ; Oxygen (S88TT14065) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2018-07-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1131675-5
    ISSN 1532-8511 ; 1052-3057
    ISSN (online) 1532-8511
    ISSN 1052-3057
    DOI 10.1016/j.jstrokecerebrovasdis.2018.05.045
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