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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	Published Erratum
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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Article: Cerebral Blood Flow Autoregulation and Dysautoregulation.

Armstead, William M

Anesthesiology clinics

2016 Volume 34, Issue 3, Page(s) 465–477

Abstract: This article provides a review of cerebral autoregulation, particularly as it relates to the clinician scientist experienced in neuroscience in anesthesia and critical care. Topics covered are biological mechanisms; methods used for assessment of ... ...

Abstract	This article provides a review of cerebral autoregulation, particularly as it relates to the clinician scientist experienced in neuroscience in anesthesia and critical care. Topics covered are biological mechanisms; methods used for assessment of autoregulation; effects of anesthetics; role in control of cerebral hemodynamics in health and disease; and emerging areas, such as role of age and sex in contribution to dysautoregulation. Emphasis is placed on bidirectional translational research wherein the clinical informs the study design of basic science studies, which, in turn, informs the clinical to result in development of improved therapies for treatment of central nervous system conditions.
MeSH term(s)	Anesthetics/pharmacology ; Animals ; Brain Injuries, Traumatic/physiopathology ; Cerebrovascular Circulation/physiology ; Extracellular Signal-Regulated MAP Kinases/physiology ; Homeostasis/drug effects ; Homeostasis/physiology ; Humans ; Intracranial Pressure
Chemical Substances	Anesthetics ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2228899-5
ISSN	2210-3538 ; 1932-2275 ; 0889-8537
ISSN (online)	2210-3538
ISSN	1932-2275 ; 0889-8537
DOI	10.1016/j.anclin.2016.04.002
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Article ; Online: Translational approach towards determining the role of cerebral autoregulation in outcome after traumatic brain injury.

Armstead, William M / Vavilala, Monica S

Experimental neurology

2019 Volume 317, Page(s) 291–297

Abstract: Cerebral autoregulation is impaired after traumatic brain injury (TBI), contributing to poor outcome. In the context of the neurovascular unit, cerebral autoregulation contributes to neuronal cell integrity and clinically Glasgow Coma Scale is correlated ...

Abstract	Cerebral autoregulation is impaired after traumatic brain injury (TBI), contributing to poor outcome. In the context of the neurovascular unit, cerebral autoregulation contributes to neuronal cell integrity and clinically Glasgow Coma Scale is correlated to intactness of autoregulation after TBI. Cerebral Perfusion Pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP) and thereby limit impairment of cerebral autoregulation and neurological deficits. However, current vasoactive agent choice used to elevate MAP to increase CPP after TBI is variable. Vasoactive agents, such as phenylephrine, dopamine, norepinephrine, and epinephrine, clinically have not sufficiently been compared regarding effect on CPP, autoregulation, and survival after TBI. The cerebral effects of these clinically commonly used vasoactive agents are incompletely understood. This review will describe translational studies using a more human like animal model (the pig) of TBI to identify better therapeutic strategies to improve outcome post injury. These studies also investigated the role of age and sex in outcome and mechanism(s) involved in improvement of outcome in the setting of TBI. Additionally, this review considers use of inhaled nitric oxide as a novel neuroprotective strategy in treatment of TBI.
MeSH term(s)	Animals ; Brain Injuries, Traumatic/physiopathology ; Cerebrovascular Circulation/physiology ; Disease Models, Animal ; Homeostasis/physiology ; Humans ; Recovery of Function/physiology ; Swine ; Translational Research, Biomedical
Language	English
Publishing date	2019-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2019.03.015
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Zs.A 184: Show issues

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Article ; Online: Improving Understanding and Outcomes of Traumatic Brain Injury Using Bidirectional Translational Research.

Armstead, William M / Vavilala, Monica S

Journal of neurotrauma

2019 Volume 37, Issue 22, Page(s) 2372–2380

Abstract: Recent clinical trials in traumatic brain injury (TBI) have failed to demonstrate therapeutic effects even when there appears to be good evidence for efficacy in one or more appropriate pre-clinical models. While existing animal models mimic the injury, ... ...

Abstract	Recent clinical trials in traumatic brain injury (TBI) have failed to demonstrate therapeutic effects even when there appears to be good evidence for efficacy in one or more appropriate pre-clinical models. While existing animal models mimic the injury, difficulties in translating promising therapeutics are exacerbated by the lack of alignment of discrete measures of the underlying injury pathology between the animal models and human subjects. To address this mismatch, we have incorporated reverse translation of bedside experience to inform pre-clinical studies in a large animal (pig) model of TBI that mirror practical clinical assessments. 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) and thereby limit impairment of cerebral autoregulation and neurological deficits. Vasoactive agents clinically used to elevate MAP to increase CPP after TBI, such as phenylephrine (Phe), dopamine (DA), norepinephrine (NE), and epinephrine (EPI), however, have not been compared sufficiently regarding effect on CPP, autoregulation, and survival after TBI, and clinically, current vasoactive agent use is variable. The cerebral effects of these clinically commonly used vasoactive agents are not known. This review will emphasize pediatric work and will describe bidirectional translational studies using a more human-like animal model of TBI to identify better therapeutic strategies to improve outcome post-injury. These studies in addition investigated the mechanism(s) involved in improvement of outcome in the setting of TBI.
MeSH term(s)	Animals ; Brain Injuries, Traumatic ; Disease Models, Animal ; Humans ; Mice ; Swine ; Translational Medical Research
Language	English
Publishing date	2019-06-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2018.6119
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Article ; Online: Propranolol protects cerebral autoregulation and reduces hippocampal neuronal cell death through inhibition of interleukin-6 upregulation after traumatic brain injury in pigs.

Armstead, William M / Vavilala, Monica S

British journal of anaesthesia

2019 Volume 123, Issue 5, Page(s) 610–617

Abstract: Background: Traumatic brain injury (TBI) is associated with reduced cerebral blood flow and impaired autoregulation after TBI, which may lead to poor outcome. Clinical evidence has implicated neurological injuries and associated neuroinflammation as ... ...

Abstract	Background: Traumatic brain injury (TBI) is associated with reduced cerebral blood flow and impaired autoregulation after TBI, which may lead to poor outcome. Clinical evidence has implicated neurological injuries and associated neuroinflammation as causes of cardiac dysfunction. Studies on newborn pigs show an association of elevated catecholamines with a sex-dependent impairment of cerebral autoregulation after TBI. One strategy to decrease sympathetic hyperactivity is pharmacological intervention with beta blockade. We tested the hypothesis that propranolol would prevent the impairment of cerebral autoregulation and tissue changes after TBI via inhibition of interleukin-6 (IL-6) upregulation. Methods: Using newborn pigs of both sexes equipped with a closed cranial window, TBI was induced via lateral fluid percussion injury. Propranolol was administered at 1 h post-TBI. Analyses included cerebral autoregulation (pial artery reactivity) before and 4 h post-TBI, CSF IL-6 analysed (enzyme-linked immunosorbent assay), and histopathology at 4 h post-TBI. Results: Propranolol administration prevented impairment of hypotensive dilation in both male and female newborn pigs after fluid percussion injury, which was paralleled by reduced upregulation of IL-6 in the CSF. Moreover, propranolol prevented neuronal cell death in cornu amonis (CA)1 and CA3 hippocampus equivalently in male and female pigs after TBI. Papaverine-induced dilation was unchanged by TBI and propranolol. Conclusions: These data indicate that sympathetic hyperactivity noted after TBI can be limited by propranolol administration to result in improved brain outcome post-injury via block of IL-6 upregulation, and this effect is irrespective of sex.
MeSH term(s)	Adrenergic beta-Antagonists/pharmacology ; Animals ; Animals, Newborn ; Brain Injuries, Traumatic/drug therapy ; Brain Injuries, Traumatic/pathology ; Brain Injuries, Traumatic/physiopathology ; Cell Death/drug effects ; Disease Models, Animal ; Female ; Hippocampus/drug effects ; Hippocampus/physiology ; Homeostasis/drug effects ; Homeostasis/physiology ; Interleukin-6/antagonists & inhibitors ; Male ; Neurons/drug effects ; Propranolol/pharmacology ; Swine ; Up-Regulation/drug effects
Chemical Substances	Adrenergic beta-Antagonists ; Interleukin-6 ; Propranolol (9Y8NXQ24VQ)
Language	English
Publishing date	2019-09-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80074-0
ISSN	1471-6771 ; 0007-0912
ISSN (online)	1471-6771
ISSN	0007-0912
DOI	10.1016/j.bja.2019.07.017
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Article ; Online: Cerebral Perfusion Pressure Directed-Therapy Modulates Cardiac Dysfunction After Traumatic Brain Injury to Influence Cerebral Autoregulation in Pigs.

Armstead, William M / Vavilala, Monica S

Neurocritical care

2019 Volume 31, Issue 3, Page(s) 476–485

Abstract: Background: Traumatic brain injury (TBI) is an important contributor to morbidity and mortality. Low cerebral perfusion pressure (CPP, mean arterial pressure [MAP] minus intracranial pressure) after TBI is associated with cerebral ischemia, impaired ... ...

Abstract	Background: Traumatic brain injury (TBI) is an important contributor to morbidity and mortality. Low cerebral perfusion pressure (CPP, mean arterial pressure [MAP] minus intracranial pressure) after TBI is associated with cerebral ischemia, impaired cerebral autoregulation, and poor outcomes. Normalization of CPP and limitation of cerebral autoregulation impairment is a key therapeutic goal. However, some vasoactive agents used to elevate MAP such as phenylephrine (Phe) improve outcome in females but not male piglets after TBI while dopamine (DA) does so in both sexes. Clinical evidence has implicated neurological injuries as a cause of cardiac dysfunction, and we recently described cardiac dysfunction after TBI. Cardiac dysfunction may, in turn, influence brain health. One mechanism of myocyte injury may involve catecholamine excess. We therefore tested the hypothesis that TBI caused cardiac dysfunction and catecholamine excess which may reciprocally be modulated by vasoactive agent choice to normalize CPP and prevent impairment of cerebral autoregulation after injury. Methods: TBI was produced in anesthetized pigs equipped with a closed cranial window, and Phe or DA administered to normalize CPP. Results: Plasma cardiac enzymes troponin and creatine kinase and catecholamines epinephrine and norepinephrine were elevated by TBI, such release potentiated by Phe in males but blocked in female piglets and blocked in both sexes after DA. Cerebral autoregulation was impaired after TBI, worsened by Phe in males but protected in females and males treated with DA. Papaverine-induced dilation was unchanged by fluid percussion brain injury, DA, and Phe. Conclusions: These data indicate that pressor choice in elevation of CPP is important in limiting cardiac dysfunction and suggest that DA protects cerebral autoregulation in both sexes via reduction of cardiac biomarkers of injury and catecholamines released after TBI.
MeSH term(s)	Animals ; Animals, Newborn ; Arterial Pressure/drug effects ; Brain Injuries, Traumatic/blood ; Brain Injuries, Traumatic/physiopathology ; Cerebrovascular Circulation/drug effects ; Creatine Kinase, MB Form/blood ; Creatine Kinase, MB Form/drug effects ; Dopamine/pharmacology ; Epinephrine/blood ; Female ; Heart/drug effects ; Heart/physiopathology ; Homeostasis/drug effects ; Intracranial Pressure ; Male ; Norepinephrine/blood ; Papaverine/pharmacology ; Phenylephrine/pharmacology ; Random Allocation ; Sex Factors ; Sus scrofa ; Swine ; Sympathomimetics/pharmacology ; Troponin I/blood ; Troponin I/drug effects ; Vasodilator Agents/pharmacology
Chemical Substances	Sympathomimetics ; Troponin I ; Vasodilator Agents ; Phenylephrine (1WS297W6MV) ; Papaverine (DAA13NKG2Q) ; Creatine Kinase, MB Form (EC 2.7.3.2) ; Dopamine (VTD58H1Z2X) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2019-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2381896-7
ISSN	1556-0961 ; 1541-6933
ISSN (online)	1556-0961
ISSN	1541-6933
DOI	10.1007/s12028-019-00735-2
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Article ; Online: Retraction Note: Sex and age differences in phenylephrine mechanisms and outcomes after piglet brain injury.

Curvello, Victor / Hekierski, Hugh / Riley, John / Vavilala, Monica / Armstead, William M

Pediatric research

2022 Volume 92, Issue 4, Page(s) 1200

Language	English
Publishing date	2022-08-17
Publishing country	United States
Document type	Retraction of Publication
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/s41390-022-02248-9
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Zs.A 564: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Nociceptin/orphanin phenylalanine glutamine (FQ) receptor and cardiovascular disease.

Armstead, William M

Cardiovascular therapeutics

2011 Volume 29, Issue 1, Page(s) 23–28

Abstract: Nociceptin/Orphanin FQ (N/OFQ) is the endogenous ligand for the N/OFQ receptor. N/OFQ acts directly on blood vessels to elicit vasodilation. This review will describe the peripheral cardiovascular effects of N/OFQ observed in studies conducted in vitro ... ...

Abstract	Nociceptin/Orphanin FQ (N/OFQ) is the endogenous ligand for the N/OFQ receptor. N/OFQ acts directly on blood vessels to elicit vasodilation. This review will describe the peripheral cardiovascular effects of N/OFQ observed in studies conducted in vitro and in vivo, along with those designed to characterize systemic cardiovascular effects resulting from direct injection into brain tissue. Emphasis is placed on the cerebrovascular action of N/OFQ and its function considered in the setting of central nervous system (CNS) pathology. Although N/OFQ is unlikely to cross the blood-brain barrier because of its size, use of N/OFQ antagonists to alleviate the potentially deleterious action of centrally released N/OFQ may be of therapeutic importance in treatment of cerebral ischemia of diverse origin, such as stroke and traumatic brain injury. Targeting N/OFQ may also be of therapeutic importance in alleviating the hyperemia and pain associated with joint inflammation.
MeSH term(s)	Amino Acid Sequence ; Animals ; Brain Injuries/drug therapy ; Brain Injuries/pathology ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/etiology ; Humans ; Hypoxia-Ischemia, Brain/drug therapy ; Hypoxia-Ischemia, Brain/pathology ; Molecular Sequence Data ; Narcotic Antagonists ; Neurotransmitter Agents/secretion ; Receptors, Opioid/physiology
Chemical Substances	Narcotic Antagonists ; Neurotransmitter Agents ; Receptors, Opioid ; nociceptin receptor
Language	English
Publishing date	2011-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2428378-2
ISSN	1755-5922 ; 1755-5914
ISSN (online)	1755-5922
ISSN	1755-5914
DOI	10.1111/j.1755-5922.2010.00241.x
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Zs.A 2474: 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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