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Article ; Online: Retraction notice to "Dopamine protects cerebral autoregulation and prevents hippocampal necrosis after traumatic brain injury via block of ERK MAPK in juvenile pigs" [Brain Res. 1670 (2017) 118-124].

Curvello, Victor / Hekierski, Hugh / Pastor, Philip / Vavilala, Monica S / Armstead, William M

2024 Volume 1836, Page(s) 148903

Language	English
Publishing date	2024-04-25
Publishing country	Netherlands
Document type	Journal Article ; Retraction of Publication
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2024.148903
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Article ; Online: Retraction Note: Inhaled Nitric Oxide Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis After Traumatic Brain Injury Through Inhibition of ET-1, ERK MAPK and IL-6 Upregulation in Pigs.

Curvello, Victor / Pastor, Philip / Hekierski, Hugh / Armstead, William M

Neurocritical care

2022 Volume 38, Issue 1, Page(s) 219

Language	English
Publishing date	2022-11-22
Publishing country	United States
Document type	Retraction of Publication
ZDB-ID	2381896-7
ISSN	1556-0961 ; 1541-6933
ISSN (online)	1556-0961
ISSN	1541-6933
DOI	10.1007/s12028-022-01640-x
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Zs.A 6538: Show issues

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Article ; Online: Inhaled nitric oxide protects cerebral autoregulation through prevention of impairment of ATP and calcium sensitive K channel mediated cerebrovasodilation after traumatic brain injury.

Pastor, Philip / Curvello, Victor / Hekierski, Hugh / Armstead, William M

Brain research

2019 Volume 1711, Page(s) 1–6

Abstract: Hypotension and low cerebral perfusion pressure are associated with low cerebral blood flow, cerebral ischemia, and poor outcomes after traumatic brain injury (TBI). Cerebral autoregulation is impaired after TBI, contributing to poor outcome. In prior ... ...

Abstract	Hypotension and low cerebral perfusion pressure are associated with low cerebral blood flow, cerebral ischemia, and poor outcomes after traumatic brain injury (TBI). Cerebral autoregulation is impaired after TBI, contributing to poor outcome. In prior studies, ERK mitogen activated protein kinase (MAPK) and ET-1 had been observed to be upregulated and contribute to impairment of cerebral autoregulation and histopathology after fluid percussion brain injury (FPI). Activation of ATP and Calcium sensitive (Katp and Kca) channels produce cerebrovasodilation and contribute to autoregulation, both impaired after TBI. Upregulation of ERK MAPK and endothelin-1 (ET-1) produces K channel function impairment after CNS injury. Inhaled nitric oxide (iNO) has recently been observed to prevent impairment of cerebral autoregulation and hippocampal CA1 and CA3 neuronal cell necrosis after FPI via block of upregulation of ERK MAPK and ET-1. We presently investigated whether iNO prevented impairment of Katp and Kca-mediated cerebrovasodilation after FPI in pigs equipped with a closed cranial window. Results show that pial artery dilation in response to the Katp agonist cromakalim, the Kca agonist NS1619, PGE2 and the NO releaser sodium nitroprusside (SNP) were blocked by FPI, but such impairment was prevented by iNO administered at 2 h post injury. Protection lasted for at least 1 h after iNO administration was stopped. Using vasodilaton as an index of function, these data indicate that iNO prevents impairment of cerebral autoregulation and limits histopathology after TBI through protection of K channel function via blockade of ERK MAPK and ET-1.
MeSH term(s)	Adenosine Triphosphate/pharmacology ; Animals ; Animals, Newborn ; Brain Injuries, Traumatic/drug therapy ; Brain Injuries, Traumatic/pathology ; Calcium/metabolism ; Calcium Channels/metabolism ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Circulation/physiology ; Endothelin-1/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Homeostasis/drug effects ; Male ; Nitric Oxide/metabolism ; Nitric Oxide/pharmacology ; Potassium Channels, Calcium-Activated/drug effects ; Swine ; Vasodilation/drug effects ; Vasodilator Agents/pharmacology
Chemical Substances	Calcium Channels ; Endothelin-1 ; Potassium Channels, Calcium-Activated ; Vasodilator Agents ; Nitric Oxide (31C4KY9ESH) ; Adenosine Triphosphate (8L70Q75FXE) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-01-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2019.01.008
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Zs.A 161: Show issues

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Article ; Online: Inhaled Nitric Oxide Protects Cerebral Autoregulation and Reduces Hippocampal Neuronal Cell Necrosis after Traumatic Brain Injury in Newborn and Juvenile Pigs.

Hekierski, Hugh / Pastor, Philip / Curvello, Victor / Armstead, William M

Journal of neurotrauma

2018 Volume 36, Issue 4, Page(s) 630–638

Abstract: Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Cerebral blood flow (CBF) is reduced and autoregulation is impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure (CPP) ...

Abstract	Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Cerebral blood flow (CBF) is reduced and autoregulation is impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). In prior studies of male and female newborn and juvenile pigs, we observed that phenylephrine, norepinephrine, epinephrine, and dopamine demonstrated different sex- and age-dependent abilities to prevent impairment of cerebral autoregulation and limit histopathology after TBI, despite equivalent CPP values. This observation complicated treatment choice. Alternatively, administration of a cerebral vasodilator may improve cerebral hemodynamics after TBI by increasing CBF. In prior studies, intravenous sodium nitroprusside, a nitric oxide (NO) releaser, elevated CBF after TBI but failed to prevent impairment of cerebral autoregulation due to a confounding decrease in MAP, which lowered CPP. We presently test the hypothesis that inhaled NO (iNO) will protect cerebral autoregulation and prevent hippocampal histopathology after TBI. Results show that iNO administered at 30 min or 2 h after TBI protected cerebral autoregulation and prevented neuronal cell necrosis in CA1 and CA3 hippocampus equivalently in male and female newborn and juvenile pigs without change in MAP. Protection lasted for at least 2 h after iNO administration was stopped. Papaverine-induced dilation was unchanged by TBI and iNO. These data indicate that iNO offers the opportunity to have a single therapeutic that uniformly protects autoregulation and limits hippocampal neuronal cell necrosis across both ages and sexes.
MeSH term(s)	Animals ; Animals, Newborn ; Brain/blood supply ; Brain/drug effects ; Brain/pathology ; Brain Injuries, Traumatic/pathology ; Cerebrovascular Circulation/drug effects ; Female ; Homeostasis/drug effects ; Male ; Necrosis/pathology ; Neurons/drug effects ; Neurons/pathology ; Nitric Oxide/pharmacology ; Swine ; Vasodilator Agents/pharmacology
Chemical Substances	Vasodilator Agents ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2018-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2018.5824
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Zs.A 2016: Show issues

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Article ; Online: Release of IL-6 After Stroke Contributes to Impaired Cerebral Autoregulation and Hippocampal Neuronal Necrosis Through NMDA Receptor Activation and Upregulation of ET-1 and JNK.

Armstead, William M / Hekierski, Hugh / Pastor, Philip / Yarovoi, Serge / Higazi, Abd Al-Roof / Cines, Douglas B

Translational stroke research

2018 Volume 10, Issue 1, Page(s) 104–111

Abstract: The sole FDA-approved drug treatment for ischemic stroke is tissue-type plasminogen activator (tPA). However, upregulation of JNK mitogen-activated protein kinase (MAPK) and endothelin 1 (ET-1) by tPA after stroke contributes to impaired cerebrovascular ... ...

Abstract	The sole FDA-approved drug treatment for ischemic stroke is tissue-type plasminogen activator (tPA). However, upregulation of JNK mitogen-activated protein kinase (MAPK) and endothelin 1 (ET-1) by tPA after stroke contributes to impaired cerebrovascular autoregulation. Wild-type (wt) tPA can bind to the lipoprotein-related receptor (LRP), which mediates vasodilation, or NMDA receptors (NMDA-Rs), exacerbating vasoconstriction. Elevations in IL-6, a marker of inflammation that accompanies stroke, are reported to be an adverse prognostic factor. We hypothesized that IL-6 released into CSF after stroke by wt-tPA through activation of NMDA-Rs and upregulation of ET-1 and JNK contribute to impairment of cerebrovascular autoregulation and increased histopathology. Results show that IL-6 was increased post stroke in pigs, which was increased further by wt-tPA. Co-administration of the IL-6 antagonist LMT-28 with wt-tPA prevented impairment of cerebrovascular autoregulation and necrosis of hippocampal cells. wt-tPA co-administered with the JNK inhibitor SP 600125 and the ET-1 antagonist BQ 123 blocked stroke-induced elevation of IL-6. Co-administration of LMT-28 with wt-tPA blocked the augmentation of JNK and ET-1 post stroke. In conclusion, IL-6 released after stroke, which is enhanced by wt-tPA through activation of NMDA-Rs and upregulation of ET-1 and JNK, impairs cerebrovascular autoregulation and increases histopathology. Strategies that promote fibrinolysis while limiting activation of NMDA-Rs and upregulation of IL-6 may improve the benefit/risk ratio compared to wt-tPA in treatment of stroke.
MeSH term(s)	Animals ; Anthracenes/therapeutic use ; Cerebral Cortex/physiopathology ; Disease Models, Animal ; Endothelin-1 ; Hippocampus/pathology ; Homeostasis/physiology ; Interleukin-6/metabolism ; Necrosis/etiology ; Oxazolidinones/therapeutic use ; Random Allocation ; Receptors, N-Methyl-D-Aspartate ; Signal Transduction ; Stroke/complications ; Stroke/drug therapy ; Stroke/metabolism ; Stroke/pathology ; Swine ; Tissue Plasminogen Activator/therapeutic use ; Up-Regulation
Chemical Substances	Anthracenes ; Endothelin-1 ; Interleukin-6 ; LMT-28 ; Oxazolidinones ; Receptors, N-Methyl-D-Aspartate ; pyrazolanthrone (1TW30Y2766) ; Tissue Plasminogen Activator (EC 3.4.21.68)
Language	English
Publishing date	2018-02-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541897-X
ISSN	1868-601X ; 1868-4483
ISSN (online)	1868-601X
ISSN	1868-4483
DOI	10.1007/s12975-018-0617-z
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Article ; Online: Inhaled Nitric Oxide Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis After Traumatic Brain Injury Through Inhibition of ET-1, ERK MAPK and IL-6 Upregulation in Pigs.

Curvello, Victor / Pastor, Philip / Hekierski, Hugh / Armstead, William M

publication RETRACTED

Neurocritical care

2016 Volume 30, Issue 2, Page(s) 467–477

Abstract: Objective: Traumatic brain injury (TBI) is an important contributor to morbidity and mortality. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Extracellular signal-related kinase (ERK) mitogen activated protein kinase (MAPK) ...

Abstract	Objective: Traumatic brain injury (TBI) is an important contributor to morbidity and mortality. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Extracellular signal-related kinase (ERK) mitogen activated protein kinase (MAPK) and ET-1 are upregulated and contribute to impairment of cerebral autoregulation and histopathology after porcine fluid percussion brain injury (FPI). Recent studies show that inhaled nitric oxide (iNO) prevents impairment of cerebral autoregulation and histopathology after FPI in pigs. Unrelated studies indicated an association between ERK and increased IL-6 after FPI. However, the role of IL-6 in central nervous system (CNS) pathology is not well understood. We investigated whether iNO protects autoregulation and limits histopathology after FPI in pigs due to modulation of brain injury associated upregulation of ET-1, ERK MAPK, and IL-6. Methods: Lateral FPI was produced in anesthetized pigs equipped with a closed cranial window and iNO administered at 30 min or 2 h post injury. Results: CSF ET-1, ERK MAPK, and IL-6 were increased by FPI, but release was blocked by iNO administered at 30 min or 2 h after TBI. The IL-6 antagonist LMT-28 prevented impairment of cerebral autoregulation and hippocampal CA1 and CA3 neuronal necrosis after FPI. Papaverine induced dilation was unchanged by FPI and LMT-28. Protection lasted for at least 2 h after iNO administration was stopped. Conclusions: These data indicate that iNO protects cerebral autoregulation and reduces hippocampal necrosis after traumatic brain injury through inhibition of ET-1, ERK MAPK, and IL-6 upregulation in pigs.
MeSH term(s)	Administration, Inhalation ; Animals ; Animals, Newborn ; Brain Injuries, Traumatic/cerebrospinal fluid ; Brain Injuries, Traumatic/drug therapy ; Brain Injuries, Traumatic/pathology ; Disease Models, Animal ; Endothelin-1/cerebrospinal fluid ; Endothelin-1/drug effects ; Extracellular Signal-Regulated MAP Kinases/cerebrospinal fluid ; Extracellular Signal-Regulated MAP Kinases/drug effects ; Female ; Hippocampus/drug effects ; Hippocampus/pathology ; Homeostasis/drug effects ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/cerebrospinal fluid ; Male ; Necrosis/pathology ; Necrosis/prevention & control ; Nitric Oxide/administration & dosage ; Nitric Oxide/pharmacology ; Oxazolidinones/pharmacology ; Papaverine/pharmacology ; Protein Synthesis Inhibitors/pharmacology ; Signal Transduction/drug effects ; Swine ; Up-Regulation/drug effects ; Vasodilator Agents/administration & dosage ; Vasodilator Agents/pharmacology
Chemical Substances	Endothelin-1 ; Interleukin-6 ; LMT-28 ; Oxazolidinones ; Protein Synthesis Inhibitors ; Vasodilator Agents ; Nitric Oxide (31C4KY9ESH) ; Papaverine (DAA13NKG2Q) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2016-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Retracted Publication
ZDB-ID	2381896-7
ISSN	1556-0961 ; 1541-6933
ISSN (online)	1556-0961
ISSN	1541-6933
DOI	10.1007/s12028-018-0638-1
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Zs.A 6538: Show issues

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Article ; Online: Dopamine protects cerebral autoregulation and prevents hippocampal necrosis after traumatic brain injury via block of ERK MAPK in juvenile pigs.

Curvello, Victor / Hekierski, Hugh / Pastor, Philip / Vavilala, Monica S / Armstead, William M

publication RETRACTED

Brain research

2017 Volume 1670, Page(s) 118–124

Abstract: Traumatic brain injury (TBI) contributes to morbidity in children, and more boys experience TBI. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Cerebral Perfusion Pressure (CPP) is often normalized by use of vasoactive ... ...

Abstract	Traumatic brain injury (TBI) contributes to morbidity in children, and more boys experience TBI. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Cerebral Perfusion Pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). In prior studies of newborn and juvenile pigs, vasoactive agent choice influenced outcome after TBI as a function of age and sex, with none protecting cerebral autoregulation in both ages and sexes. Dopamine (DA) prevents impairment of cerebral autoregulation in male and female newborn pigs via inhibition of upregulation of ERK mitogen activated protein kinase (MAPK) after fluid percussion injury (FPI). We investigated whether DA protects autoregulation and limits histopathology after FPI in juvenile pigs and the role of ERK in that outcome. Results show that DA protects autoregulation in both male and female juvenile pigs after FPI. Papaverine induced dilation was unchanged by FPI and DA. DA blunted ERK MAPK and prevented loss of neurons in CA1 and CA3 hippocampus of males and females after FPI. These data indicate that DA protects autoregulation and limits hippocampal neuronal cell necrosis via block of ERK after FPI in male and female juvenile pigs. Of the vasoactive agents prior investigated, including norepinephrine, epinephrine, and phenylephrine, DA is the only one demonstrated to improve outcome after TBI in both sexes and ages. These data suggest that DA should be considered as a first line treatment to protect cerebral autoregulation and promote cerebral outcomes in pediatric TBI irrespective of age and sex.
MeSH term(s)	Animals ; Brain Injuries/metabolism ; Brain Injuries, Traumatic/drug therapy ; Cerebrovascular Circulation/physiology ; Dopamine/metabolism ; Dopamine/pharmacology ; Epinephrine/pharmacology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Hippocampus/drug effects ; Hippocampus/metabolism ; Homeostasis/drug effects ; Homeostasis/physiology ; MAP Kinase Signaling System/drug effects ; Male ; Mitogen-Activated Protein Kinase Kinases ; Mitogen-Activated Protein Kinases/drug effects ; Mitogen-Activated Protein Kinases/metabolism ; Necrosis/metabolism ; Necrosis/prevention & control ; Norepinephrine/pharmacology ; Phenylephrine/pharmacology ; Swine/metabolism ; Swine/physiology ; Up-Regulation/drug effects ; Vasoconstrictor Agents/pharmacology ; Vasodilation/drug effects
Chemical Substances	Vasoconstrictor Agents ; Phenylephrine (1WS297W6MV) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Dopamine (VTD58H1Z2X) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2017-06-15
Publishing country	Netherlands
Document type	Journal Article ; Retracted Publication
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2017.06.010
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