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Pathophysiology of blood-brain barrier in brain injury in cold and hot environments: Novel drug targets for neuroprotection

dc.contributor.authorSharma H.S.
dc.contributor.authorMuresanu D.F.
dc.contributor.authorLafuente J.V.
dc.contributor.authorNozari A.
dc.contributor.authorPatnaik R.
dc.contributor.authorSkaper S.D.
dc.contributor.authorSharma A.
dc.date.accessioned2020-09-02T22:28:13Z
dc.date.available2020-09-02T22:28:13Z
dc.date.issued2016
dc.identifier10.2174/1871527315666160902145145
dc.identifier.citation15, 9, 1045-1071
dc.identifier.issn18715273
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6246
dc.descriptionThe blood-brain barrier (BBB) plays a pivotal role in the maintenance of central nervous system function in health and disease. Thus, in almost all neurodegenerative, traumatic or metabolic insults BBB breakdown occurs, allowing entry of serum proteins into the brain fluid microenvironment with subsequent edema formation and cellular injury. Accordingly, pharmacological restoration of BBB function will lead to neurorepair. However, brain injury which occurs following blast, bullet wounds, or knife injury appears to initiate different sets of pathophysiological responses. Moreover, other local factors at the time of injury such as cold or elevated ambient temperatures could also impact the final outcome. Obviously, drug therapy applied to different kinds of brain trauma occurring at either cold or hot environments may respond differently. This is largely due to the fact that internal defense mechanisms of the brain, gene expression, release of neurochemicals and binding of drugs to specific receptors are affected by external ambient temperature changes. These factors may also affect BBB function and development of edema formation after brain injury. In this review, the effects of seasonal exposure to heat and cold on traumatic brain injury using different models i.e., concussive brain injury and cerebral cortical lesion, on BBB dysfunction in relation to drug therapy are discussed. Our observations clearly suggest that closed head injury and open brain injury are two different entities and the external hot or cold environments affect both of them remarkably. Thus, effective pharmacological therapeutic strategies should be designed with these views in mind, as military personnel often experience blunt or penetrating head injuries in either cold or hot environments. © 2016, Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers B.V.
dc.subjectAmbient temperature
dc.subjectBlood-brain barrier
dc.subjectBlunt head injury
dc.subjectBrain edema
dc.subjectBrain pathology
dc.subjectCognitive dysfunction
dc.subjectCold exposure
dc.subjectConcussion
dc.subjectCortical injury
dc.subjectDrug therapy
dc.subjectHot environment
dc.subjectPenetrating brain injury
dc.subjectSeasonal variations
dc.subjectTraumatic brain injury
dc.subjectantioxidant
dc.subjectbrain derived neurotrophic factor
dc.subjectcerebrolysin
dc.subjectciliary neurotrophic factor
dc.subjectcimetidine
dc.subjectcyclic GMP
dc.subjectcyproheptadine
dc.subjectdynorphin A
dc.subjectfenclonine
dc.subjectglial cell line derived neurotrophic factor
dc.subjectheat shock protein 72
dc.subjectheme oxygenase 2
dc.subjecthistamine H2 receptor
dc.subjecthistamine H3 receptor
dc.subjectibuprofen
dc.subjectindometacin
dc.subjectmepyramine
dc.subjectmu opiate receptor
dc.subjectnaloxone
dc.subjectneutralizing antibody
dc.subjectnitric oxide synthase
dc.subjectparacetamol
dc.subjectphosphodiesterase inhibitor
dc.subjectprotein antibody
dc.subjectprotein c fos
dc.subjectserotonin
dc.subjectserotonin 2C receptor
dc.subjectsomatomedin C
dc.subjecttumor necrosis factor
dc.subjectneuroprotective agent
dc.subjectblood brain barrier
dc.subjectbrain blood flow
dc.subjectbrain cortex lesion
dc.subjectbrain edema
dc.subjectbrain injury
dc.subjectcognitive defect
dc.subjectcold exposure
dc.subjectcold stress
dc.subjectconcussion
dc.subjectdrug delivery system
dc.subjectenvironmental temperature
dc.subjectfootprint test
dc.subjectfunctional status assessment
dc.subjectgene expression
dc.subjectglia cell
dc.subjectgrid walking test
dc.subjectgunshot injury
dc.subjecthead injury
dc.subjecthuman
dc.subjecthyperglycemia
dc.subjecthyperthermia
dc.subjectimmunoreactivity
dc.subjectknife cut
dc.subjectmembrane permeability
dc.subjectmicroenvironment
dc.subjectnerve cell lesion
dc.subjectneurologic disease assessment
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectpenetrating trauma
dc.subjectprotein expression
dc.subjectReview
dc.subjectrotarod test
dc.subjectseasonal variation
dc.subjectsoldier
dc.subjectthermal exposure
dc.subjecttraumatic brain injury
dc.subjectanimal
dc.subjectblood brain barrier
dc.subjectBrain Injuries
dc.subjectcold
dc.subjectdrug effects
dc.subjectenvironment
dc.subjectheat
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectAnimals
dc.subjectBlood-Brain Barrier
dc.subjectBrain Injuries
dc.subjectCold Temperature
dc.subjectEnvironment
dc.subjectHot Temperature
dc.subjectHumans
dc.subjectNeuroprotective Agents
dc.titlePathophysiology of blood-brain barrier in brain injury in cold and hot environments: Novel drug targets for neuroprotection
dc.typeReview


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