FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2108769904> ?p ?o ?g. }

• W2108769904 endingPage "1873" @default.
• W2108769904 startingPage "1871" @default.
• W2108769904 abstract "Background. Central nervous system dysfunction continues to produce significant morbidity and associated mortality in patients undergoing cardiac surgery. Using a closed-chest canine cardiopulmonary bypass model, dogs underwent 2 h of hypothermic circulatory arrest (HCA) at 18°C, followed by resuscitation and recovery for 3 days. Animals were assessed functionally by a species-specific behavioral scale, histologically for patterns of selective neuronal necrosis, biochemically by analysis of microdialysis effluent, and by receptor autoradiography for N-methyl-D-aspartate (NMDA) glutamate receptor subtype expression.Results. Using a selective NMDA (glutamate) receptor antagonist (MK801) and an AMPA antagonist (NBQX), glutamate excitotoxicity in the development of HCA-induced brain injury was documented and validated. A microdialysis technique was employed to evaluate the role of nitric oxide (NO) in neuronal cell death. Arginine plus oxygen is converted to NO plus citrulline (CIT) by the action of NO synthase (nNOS). CIT recovery in the cerebrospinal fluid and from canine cortical homogenates increased during HCA and reperfusion. These studies demonstrated that neurotoxicity after HCA involves a significant and early induction of nNOS expression, and neuronal processes leading to widespread augmentation of NO production in the brain.To further investigate the production of excitatory amino acids in the brain, we hypothesized the following scenario: HCA→ ↑ glutamate, ↑ aspartate, ↑ glycine→ ↑ intracellular Ca2+→ ↑ NO + CIT. Using the same animal preparation, we demonstrated that HCA caused increased intracerebral glutamate and aspartate that persists up to 20 h post-HCA. HCA also resulted in CIT (NO) production, causing a continued and delayed neurologic injury. Confirmatory evidence of the role of NO was demonstrated by a further experiment using a specific nNOS inhibitor, 7-nitroindazole. Animals underwent 2 h of HCA, and then were evaluated both physiologically and for NO production. 7-Nitroindazole reduced CIT (NO) production by 58.4 ± 28.3%. In addition, dogs treated with this drug had superior neurologic function compared with untreated HCA controls.Conclusions. These experiments have documented the role of glutamate excitotoxicity in neurologic injury and have implicated NO as a significant neurotoxin causing necrosis and apoptosis. Continued research into the pathophysiologic mechanisms involved in cerebral injury will eventually yield a safe and reliable neuroprotectant strategy. Specific interventional agents will include glutamate receptor antagonists and specific neuronal NO synthase inhibitors." @default.
• W2108769904 created "2016-06-24" @default.
• W2108769904 creator A5014113094 @default.
• W2108769904 creator A5016635090 @default.
• W2108769904 creator A5017114335 @default.
• W2108769904 creator A5030261399 @default.
• W2108769904 creator A5048570234 @default.
• W2108769904 creator A5048940403 @default.
• W2108769904 creator A5054739785 @default.
• W2108769904 creator A5076251388 @default.
• W2108769904 creator A5077720904 @default.
• W2108769904 creator A5083890717 @default.
• W2108769904 creator A5087413391 @default.
• W2108769904 date "1999-06-01" @default.
• W2108769904 modified "2023-10-14" @default.
• W2108769904 title "Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury?" @default.
• W2108769904 cites W1965785456 @default.
• W2108769904 cites W1985529283 @default.
• W2108769904 cites W1990284918 @default.
• W2108769904 cites W231039469 @default.
• W2108769904 cites W2413221909 @default.
• W2108769904 cites W4240085224 @default.
• W2108769904 doi "https://doi.org/10.1016/s0003-4975(99)00445-2" @default.
• W2108769904 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10391329" @default.
• W2108769904 hasPublicationYear "1999" @default.
• W2108769904 type Work @default.
• W2108769904 sameAs 2108769904 @default.
• W2108769904 citedByCount "50" @default.
• W2108769904 countsByYear W21087699042012 @default.
• W2108769904 countsByYear W21087699042013 @default.
• W2108769904 countsByYear W21087699042019 @default.
• W2108769904 countsByYear W21087699042020 @default.
• W2108769904 crossrefType "journal-article" @default.
• W2108769904 hasAuthorship W2108769904A5014113094 @default.
• W2108769904 hasAuthorship W2108769904A5016635090 @default.
• W2108769904 hasAuthorship W2108769904A5017114335 @default.
• W2108769904 hasAuthorship W2108769904A5030261399 @default.
• W2108769904 hasAuthorship W2108769904A5048570234 @default.
• W2108769904 hasAuthorship W2108769904A5048940403 @default.
• W2108769904 hasAuthorship W2108769904A5054739785 @default.
• W2108769904 hasAuthorship W2108769904A5076251388 @default.
• W2108769904 hasAuthorship W2108769904A5077720904 @default.
• W2108769904 hasAuthorship W2108769904A5083890717 @default.
• W2108769904 hasAuthorship W2108769904A5087413391 @default.
• W2108769904 hasBestOaLocation W21087699041 @default.
• W2108769904 hasConcept C126322002 @default.
• W2108769904 hasConcept C160268369 @default.
• W2108769904 hasConcept C170493617 @default.
• W2108769904 hasConcept C2780076171 @default.
• W2108769904 hasConcept C2781012912 @default.
• W2108769904 hasConcept C42219234 @default.
• W2108769904 hasConcept C50156730 @default.
• W2108769904 hasConcept C529278444 @default.
• W2108769904 hasConcept C61174792 @default.
• W2108769904 hasConcept C67018056 @default.
• W2108769904 hasConcept C71924100 @default.
• W2108769904 hasConcept C98274493 @default.
• W2108769904 hasConceptScore W2108769904C126322002 @default.
• W2108769904 hasConceptScore W2108769904C160268369 @default.
• W2108769904 hasConceptScore W2108769904C170493617 @default.
• W2108769904 hasConceptScore W2108769904C2780076171 @default.
• W2108769904 hasConceptScore W2108769904C2781012912 @default.
• W2108769904 hasConceptScore W2108769904C42219234 @default.
• W2108769904 hasConceptScore W2108769904C50156730 @default.
• W2108769904 hasConceptScore W2108769904C529278444 @default.
• W2108769904 hasConceptScore W2108769904C61174792 @default.
• W2108769904 hasConceptScore W2108769904C67018056 @default.
• W2108769904 hasConceptScore W2108769904C71924100 @default.
• W2108769904 hasConceptScore W2108769904C98274493 @default.
• W2108769904 hasIssue "6" @default.
• W2108769904 hasLocation W21087699041 @default.
• W2108769904 hasLocation W21087699042 @default.
• W2108769904 hasOpenAccess W2108769904 @default.
• W2108769904 hasPrimaryLocation W21087699041 @default.
• W2108769904 hasRelatedWork W1979247955 @default.
• W2108769904 hasRelatedWork W1990201126 @default.
• W2108769904 hasRelatedWork W2000452226 @default.
• W2108769904 hasRelatedWork W2018508289 @default.
• W2108769904 hasRelatedWork W2035771032 @default.
• W2108769904 hasRelatedWork W2035909209 @default.
• W2108769904 hasRelatedWork W2049999565 @default.
• W2108769904 hasRelatedWork W2050792525 @default.
• W2108769904 hasRelatedWork W2141451366 @default.
• W2108769904 hasRelatedWork W4382601974 @default.
• W2108769904 hasVolume "67" @default.
• W2108769904 isParatext "false" @default.
• W2108769904 isRetracted "false" @default.
• W2108769904 magId "2108769904" @default.
• W2108769904 workType "article" @default.