FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1999158617> ?p ?o ?g. }

• W1999158617 endingPage "203" @default.
• W1999158617 startingPage "198" @default.
• W1999158617 abstract "Study objective To observe (1) whether the reperfusion is one of the causes underlying the development of diffuse alveolar injury following pulmonary embolism, and (2) whether polymorphonuclear leukocyte (PMN) accumulation occurs in the reperfused lobe, and (3) whether the production of superoxide is increased from cells obtained by BAL. Design The condition of pulmonary embolism was simulated by occluding the pulmonary artery branch using a balloon catheter in anesthetized closed-chest dogs. The occlusion was maintained for 24 h in the occlusion group, and a 2-h period of occlusion was followed by reperfusion in the reperfusion group. Histologic examination was performed at 24 h after occlusion in both groups (n=8). Using a different group of dogs (n=12), local cellular changes in the occluded and reperfused lobes were evaluated through BAL performed at 1, 2, and 3 h after reperfusion in the reperfusion group and at 3 h after occlusion in the occlusion group. Superoxide generation from BAL cells was measured by the chemiluminescence method. Results There was no histologic evidence of alveolar injury in the occluded lobe, but there were numerous leukocytes and erythrocytes along with exudate and damaged alveoli in the reperfused lobe. In the BAL study, the total cell counts recovered by BAL remained unchanged in all groups. However, the number of PMNs increased significantly in the late stages of reperfusion. Enhanced superoxide generation was observed in BAL cells obtained from reperfused lobe. Conclusion Reperfusion is one of the causes underlying the development of alveolar injury in pulmonary embolism by triggering immigration of PMNs to alveoli, which results in the increased superoxide generation in BAL cells. To observe (1) whether the reperfusion is one of the causes underlying the development of diffuse alveolar injury following pulmonary embolism, and (2) whether polymorphonuclear leukocyte (PMN) accumulation occurs in the reperfused lobe, and (3) whether the production of superoxide is increased from cells obtained by BAL. The condition of pulmonary embolism was simulated by occluding the pulmonary artery branch using a balloon catheter in anesthetized closed-chest dogs. The occlusion was maintained for 24 h in the occlusion group, and a 2-h period of occlusion was followed by reperfusion in the reperfusion group. Histologic examination was performed at 24 h after occlusion in both groups (n=8). Using a different group of dogs (n=12), local cellular changes in the occluded and reperfused lobes were evaluated through BAL performed at 1, 2, and 3 h after reperfusion in the reperfusion group and at 3 h after occlusion in the occlusion group. Superoxide generation from BAL cells was measured by the chemiluminescence method. There was no histologic evidence of alveolar injury in the occluded lobe, but there were numerous leukocytes and erythrocytes along with exudate and damaged alveoli in the reperfused lobe. In the BAL study, the total cell counts recovered by BAL remained unchanged in all groups. However, the number of PMNs increased significantly in the late stages of reperfusion. Enhanced superoxide generation was observed in BAL cells obtained from reperfused lobe. Reperfusion is one of the causes underlying the development of alveolar injury in pulmonary embolism by triggering immigration of PMNs to alveoli, which results in the increased superoxide generation in BAL cells." @default.
• W1999158617 created "2016-06-24" @default.
• W1999158617 creator A5000629884 @default.
• W1999158617 creator A5017739891 @default.
• W1999158617 creator A5032092158 @default.
• W1999158617 creator A5052770369 @default.
• W1999158617 creator A5058200710 @default.
• W1999158617 date "1997-01-01" @default.
• W1999158617 modified "2023-09-28" @default.
• W1999158617 title "Early Reperfusion Induces Alveolar Injury in Pulmonary Embolism" @default.
• W1999158617 cites W1908251724 @default.
• W1999158617 cites W1968110496 @default.
• W1999158617 cites W1978241642 @default.
• W1999158617 cites W2026735496 @default.
• W1999158617 cites W2049485678 @default.
• W1999158617 cites W2062462241 @default.
• W1999158617 cites W2089072733 @default.
• W1999158617 cites W2124560498 @default.
• W1999158617 cites W2133085732 @default.
• W1999158617 cites W2168913827 @default.
• W1999158617 cites W2238950535 @default.
• W1999158617 cites W2282794693 @default.
• W1999158617 cites W2284650314 @default.
• W1999158617 doi "https://doi.org/10.1378/chest.111.1.198" @default.
• W1999158617 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8996017" @default.
• W1999158617 hasPublicationYear "1997" @default.
• W1999158617 type Work @default.
• W1999158617 sameAs 1999158617 @default.
• W1999158617 citedByCount "4" @default.
• W1999158617 crossrefType "journal-article" @default.
• W1999158617 hasAuthorship W1999158617A5000629884 @default.
• W1999158617 hasAuthorship W1999158617A5017739891 @default.
• W1999158617 hasAuthorship W1999158617A5032092158 @default.
• W1999158617 hasAuthorship W1999158617A5052770369 @default.
• W1999158617 hasAuthorship W1999158617A5058200710 @default.
• W1999158617 hasConcept C126322002 @default.
• W1999158617 hasConcept C142724271 @default.
• W1999158617 hasConcept C164705383 @default.
• W1999158617 hasConcept C181199279 @default.
• W1999158617 hasConcept C2776265017 @default.
• W1999158617 hasConcept C2776268601 @default.
• W1999158617 hasConcept C2777714996 @default.
• W1999158617 hasConcept C2780114680 @default.
• W1999158617 hasConcept C2780795997 @default.
• W1999158617 hasConcept C42219234 @default.
• W1999158617 hasConcept C541997718 @default.
• W1999158617 hasConcept C55493867 @default.
• W1999158617 hasConcept C71924100 @default.
• W1999158617 hasConcept C86803240 @default.
• W1999158617 hasConceptScore W1999158617C126322002 @default.
• W1999158617 hasConceptScore W1999158617C142724271 @default.
• W1999158617 hasConceptScore W1999158617C164705383 @default.
• W1999158617 hasConceptScore W1999158617C181199279 @default.
• W1999158617 hasConceptScore W1999158617C2776265017 @default.
• W1999158617 hasConceptScore W1999158617C2776268601 @default.
• W1999158617 hasConceptScore W1999158617C2777714996 @default.
• W1999158617 hasConceptScore W1999158617C2780114680 @default.
• W1999158617 hasConceptScore W1999158617C2780795997 @default.
• W1999158617 hasConceptScore W1999158617C42219234 @default.
• W1999158617 hasConceptScore W1999158617C541997718 @default.
• W1999158617 hasConceptScore W1999158617C55493867 @default.
• W1999158617 hasConceptScore W1999158617C71924100 @default.
• W1999158617 hasConceptScore W1999158617C86803240 @default.
• W1999158617 hasIssue "1" @default.
• W1999158617 hasLocation W19991586171 @default.
• W1999158617 hasLocation W19991586172 @default.
• W1999158617 hasOpenAccess W1999158617 @default.
• W1999158617 hasPrimaryLocation W19991586171 @default.
• W1999158617 hasRelatedWork W1966635409 @default.
• W1999158617 hasRelatedWork W2038612219 @default.
• W1999158617 hasRelatedWork W2375104778 @default.
• W1999158617 hasRelatedWork W2398072084 @default.
• W1999158617 hasRelatedWork W2463152737 @default.
• W1999158617 hasRelatedWork W2475264243 @default.
• W1999158617 hasRelatedWork W2523006498 @default.
• W1999158617 hasRelatedWork W3032655376 @default.
• W1999158617 hasRelatedWork W4248907028 @default.
• W1999158617 hasRelatedWork W4290193190 @default.
• W1999158617 hasVolume "111" @default.
• W1999158617 isParatext "false" @default.
• W1999158617 isRetracted "false" @default.
• W1999158617 magId "1999158617" @default.
• W1999158617 workType "article" @default.