Inhalation gases or gaseous mediators as neuroprotectants for cerebral ischaemia

Ischaemic stroke is one of the leading causes of morbidity and mortality worldwide. While recombinant tissue plasminogen activator can be administered to produce thrombolysis and restore blood flow to the ischaemic brain, therapeutic benefit is only achieved in a fraction of the subset of patients e...

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Published inCurrent drug targets Vol. 14; no. 1; p. 56
Main Authors Sutherland, Brad A, Harrison, Joanne C, Nair, Shiva M, Sammut, Ivan A
Format Journal Article
LanguageEnglish
Published United Arab Emirates 01.01.2013
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Abstract Ischaemic stroke is one of the leading causes of morbidity and mortality worldwide. While recombinant tissue plasminogen activator can be administered to produce thrombolysis and restore blood flow to the ischaemic brain, therapeutic benefit is only achieved in a fraction of the subset of patients eligible for fibrinolytic intervention. Neuroprotective therapies attempting to restrict the extent of brain injury following cerebral ischaemia have not been successfully translated into the clinic despite overwhelming pre-clinical evidence of neuroprotection. Therefore, an adequate treatment for the majority of acute ischaemic stroke patients remains elusive. In the stroke literature, the use of therapeutic gases has received relatively little attention. Gases such as hyperbaric and normobaric oxygen, xenon, hydrogen, helium and argon all possess biological effects that have shown to be neuroprotective in pre-clinical models of ischaemic stroke. There are significant advantages to using gases including their relative abundance, low cost and feasibility for administration, all of which make them ideal candidates for a translational therapy for stroke. In addition, modulating cellular gaseous mediators including nitric oxide, carbon monoxide, and hydrogen sulphide may be an attractive option for ischaemic stroke therapy. Inhalation of these gaseous mediators can also produce neuroprotection, but this strategy remains to be confirmed as a viable therapy for ischaemic stroke. This review highlights the neuroprotective potential of therapeutic gas therapy and modulation of gaseous mediators for ischaemic stroke. The therapeutic advantages of gaseous therapy offer new promising directions in breaking the translational barrier for ischaemic stroke.
AbstractList Ischaemic stroke is one of the leading causes of morbidity and mortality worldwide. While recombinant tissue plasminogen activator can be administered to produce thrombolysis and restore blood flow to the ischaemic brain, therapeutic benefit is only achieved in a fraction of the subset of patients eligible for fibrinolytic intervention. Neuroprotective therapies attempting to restrict the extent of brain injury following cerebral ischaemia have not been successfully translated into the clinic despite overwhelming pre-clinical evidence of neuroprotection. Therefore, an adequate treatment for the majority of acute ischaemic stroke patients remains elusive. In the stroke literature, the use of therapeutic gases has received relatively little attention. Gases such as hyperbaric and normobaric oxygen, xenon, hydrogen, helium and argon all possess biological effects that have shown to be neuroprotective in pre-clinical models of ischaemic stroke. There are significant advantages to using gases including their relative abundance, low cost and feasibility for administration, all of which make them ideal candidates for a translational therapy for stroke. In addition, modulating cellular gaseous mediators including nitric oxide, carbon monoxide, and hydrogen sulphide may be an attractive option for ischaemic stroke therapy. Inhalation of these gaseous mediators can also produce neuroprotection, but this strategy remains to be confirmed as a viable therapy for ischaemic stroke. This review highlights the neuroprotective potential of therapeutic gas therapy and modulation of gaseous mediators for ischaemic stroke. The therapeutic advantages of gaseous therapy offer new promising directions in breaking the translational barrier for ischaemic stroke.
Author Sutherland, Brad A
Sammut, Ivan A
Nair, Shiva M
Harrison, Joanne C
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  organization: Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Level 7, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom. brad.sutherland@rdm.ox.ac.uk
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Snippet Ischaemic stroke is one of the leading causes of morbidity and mortality worldwide. While recombinant tissue plasminogen activator can be administered to...
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StartPage 56
SubjectTerms Administration, Inhalation
Animals
Brain Ischemia - drug therapy
Carbon Monoxide - administration & dosage
Carbon Monoxide - metabolism
Carbon Monoxide - pharmacology
Carbon Monoxide - therapeutic use
Clinical Trials as Topic
Drug Evaluation, Preclinical
Humans
Hydrogen - administration & dosage
Hydrogen - pharmacology
Hydrogen - therapeutic use
Hydrogen Sulfide - administration & dosage
Hydrogen Sulfide - metabolism
Hydrogen Sulfide - pharmacology
Hydrogen Sulfide - therapeutic use
Hyperbaric Oxygenation - methods
Neuroprotective Agents - administration & dosage
Neuroprotective Agents - metabolism
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Nitric Oxide - administration & dosage
Nitric Oxide - metabolism
Nitric Oxide - pharmacology
Nitric Oxide - therapeutic use
Noble Gases - administration & dosage
Noble Gases - pharmacology
Noble Gases - therapeutic use
Treatment Outcome
Title Inhalation gases or gaseous mediators as neuroprotectants for cerebral ischaemia
URI https://www.ncbi.nlm.nih.gov/pubmed/23170797
Volume 14
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