FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2163092377> ?p ?o ?g. }

• W2163092377 endingPage "287" @default.
• W2163092377 startingPage "273" @default.
• W2163092377 abstract "The role of endogenous nitric oxide (NO) generated by neuronal nitric oxide synthase (NOS‐1) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS‐1. Experiments were performed on awake and anaesthetized mutant and wild‐type control mice. Respiratory responses to varying levels of inspired oxygen (100, 21 and 12 % O 2 ) and carbon dioxide (3 and 5 % CO 2 balanced oxygen) were analysed. In awake animals, respiration was monitored by body plethysmograph along with oxygen consumption ( V O2 ), CO 2 production ( V CO2 ) and body temperature. In anaesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Cyclic 3′,5′‐guanosine monophosphate (cGMP) levels in the brainstem were analysed by radioimmunoassay as an index of nitric oxide generation. Unanaesthetized mutant mice exhibited greater respiratory responses during 21 and 12 % O 2 than the wild‐type controls. Respiratory responses were associated with significant decreases in oxygen consumption in both groups of mice, and the magnitude of change was greater in mutant than wild‐type mice. Changes in CO 2 production and body temperature, however, were comparable between both groups of mice. Similar augmentation of respiratory responses during hypoxia was also observed in anaesthetized mutant mice. In addition, five of the fourteen mutant mice displayed periodic oscillations in respiration (brief episodes of increases in respiratory rate and tidal phrenic nerve activity) while breathing 21 and 12 % O 2 , but not during 100 % O 2 . The time interval between the episodes decreased by reducing inspired oxygen from 21 to 12 % O 2 . Changes in arterial blood pressure and arterial blood gases were comparable at any given level of inspired oxygen between both groups of mice, indicating that changes in these variables do not account for the differences in the response to hypoxia. Respiratory responses to brief hyperoxia (Dejours test) and to cyanide, a potent chemoreceptor stimulant, were more pronounced in mutant mice, suggesting augmented peripheral chemoreceptor sensitivity. cGMP levels were elevated in the brainstem during 21 and 12 % O 2 in wild‐type but not in mutant mice, indicating decreased formation of nitric oxide in mutant mice. The magnitude of respiratory responses to hypercapnia (3 and 5 % CO 2 balanced oxygen) was comparable in both groups of mice in the awake and anaesthetized conditions. These observations suggest that the hypoxic responses were selectively augmented in mutant mice deficient in NOS‐1. Peripheral as well as central mechanisms contributed to the altered responses to hypoxia. These results support the idea that nitric oxide generated by NOS‐1 is an important physiological modulator of respiration during hypoxia." @default.
• W2163092377 created "2016-06-24" @default.
• W2163092377 creator A5015682769 @default.
• W2163092377 creator A5047410067 @default.
• W2163092377 creator A5064414704 @default.
• W2163092377 creator A5071112632 @default.
• W2163092377 date "1998-08-01" @default.
• W2163092377 modified "2023-10-15" @default.
• W2163092377 title "Altered respiratory responses to hypoxia in mutant mice deficient in neuronal nitric oxide synthase" @default.
• W2163092377 cites W1579070247 @default.
• W2163092377 cites W1923702019 @default.
• W2163092377 cites W1929009802 @default.
• W2163092377 cites W1983881147 @default.
• W2163092377 cites W1985761104 @default.
• W2163092377 cites W1990161760 @default.
• W2163092377 cites W1995379325 @default.
• W2163092377 cites W1996713672 @default.
• W2163092377 cites W1997307028 @default.
• W2163092377 cites W2003579274 @default.
• W2163092377 cites W2008346798 @default.
• W2163092377 cites W2022400183 @default.
• W2163092377 cites W2024512151 @default.
• W2163092377 cites W2032411573 @default.
• W2163092377 cites W2038691933 @default.
• W2163092377 cites W2038978204 @default.
• W2163092377 cites W2043210684 @default.
• W2163092377 cites W2051031104 @default.
• W2163092377 cites W2056955125 @default.
• W2163092377 cites W2068757065 @default.
• W2163092377 cites W2074187719 @default.
• W2163092377 cites W2078965371 @default.
• W2163092377 cites W2083853735 @default.
• W2163092377 cites W2089987432 @default.
• W2163092377 cites W2094304263 @default.
• W2163092377 cites W2097806253 @default.
• W2163092377 cites W2108999152 @default.
• W2163092377 cites W2151123925 @default.
• W2163092377 cites W2188773219 @default.
• W2163092377 cites W2247873738 @default.
• W2163092377 cites W2276086099 @default.
• W2163092377 cites W2308198663 @default.
• W2163092377 cites W2328724723 @default.
• W2163092377 cites W2343587713 @default.
• W2163092377 cites W2405079462 @default.
• W2163092377 cites W2416833789 @default.
• W2163092377 cites W2441368737 @default.
• W2163092377 cites W3023622811 @default.
• W2163092377 cites W4233998746 @default.
• W2163092377 cites W54185605 @default.
• W2163092377 doi "https://doi.org/10.1111/j.1469-7793.1998.273bi.x" @default.
• W2163092377 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2231102" @default.
• W2163092377 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9679181" @default.
• W2163092377 hasPublicationYear "1998" @default.
• W2163092377 type Work @default.
• W2163092377 sameAs 2163092377 @default.
• W2163092377 citedByCount "129" @default.
• W2163092377 countsByYear W21630923772012 @default.
• W2163092377 countsByYear W21630923772013 @default.
• W2163092377 countsByYear W21630923772014 @default.
• W2163092377 countsByYear W21630923772015 @default.
• W2163092377 countsByYear W21630923772016 @default.
• W2163092377 countsByYear W21630923772018 @default.
• W2163092377 countsByYear W21630923772019 @default.
• W2163092377 countsByYear W21630923772020 @default.
• W2163092377 countsByYear W21630923772021 @default.
• W2163092377 countsByYear W21630923772022 @default.
• W2163092377 countsByYear W21630923772023 @default.
• W2163092377 crossrefType "journal-article" @default.
• W2163092377 hasAuthorship W2163092377A5015682769 @default.
• W2163092377 hasAuthorship W2163092377A5047410067 @default.
• W2163092377 hasAuthorship W2163092377A5064414704 @default.
• W2163092377 hasAuthorship W2163092377A5071112632 @default.
• W2163092377 hasBestOaLocation W21630923771 @default.
• W2163092377 hasConcept C105702510 @default.
• W2163092377 hasConcept C123792249 @default.
• W2163092377 hasConcept C126322002 @default.
• W2163092377 hasConcept C134018914 @default.
• W2163092377 hasConcept C178790620 @default.
• W2163092377 hasConcept C182215343 @default.
• W2163092377 hasConcept C185592680 @default.
• W2163092377 hasConcept C2777037550 @default.
• W2163092377 hasConcept C2777622882 @default.
• W2163092377 hasConcept C2777953023 @default.
• W2163092377 hasConcept C2780994212 @default.
• W2163092377 hasConcept C42219234 @default.
• W2163092377 hasConcept C519581460 @default.
• W2163092377 hasConcept C534529494 @default.
• W2163092377 hasConcept C540031477 @default.
• W2163092377 hasConcept C71924100 @default.
• W2163092377 hasConcept C7836513 @default.
• W2163092377 hasConcept C8213797 @default.
• W2163092377 hasConcept C84393581 @default.
• W2163092377 hasConcept C86803240 @default.
• W2163092377 hasConceptScore W2163092377C105702510 @default.
• W2163092377 hasConceptScore W2163092377C123792249 @default.
• W2163092377 hasConceptScore W2163092377C126322002 @default.
• W2163092377 hasConceptScore W2163092377C134018914 @default.
• W2163092377 hasConceptScore W2163092377C178790620 @default.

• next