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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003322naa a2200433 4500
001oai:DiVA.org:uu-65047
003SwePub
008081017s2003 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-650472 URI
024a https://doi.org/10.1034/j.1399-6576.2003.00189.x2 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Liu, X. L.u Uppsala universitet,Institutionen för kirurgiska vetenskaper,Anaesthesiology and Intensive Care4 aut
2451 0a Differences in cerebral reperfusion and oxidative injury after cardiac arrest in pigs
264 c 2003-08-11
264 1b Wiley,c 2003
338 a print2 rdacarrier
520 a BACKGROUND: An investigation of the free radical scavenger sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) and the weak vasodilatator Tris buffer mixture (TBM) on cerebral cortical blood flow (CCBF) and the jugular bulb concentration of two eicosanoids, indicators of oxidative stress and inflammation, was undertaken in 30 anaesthetized piglets during cardiopulmonary resuscitation (CPR) and after restoration of spontaneous circulation (ROSC).METHODS: Thirty animals were subjected to 8 min of untreated circulatory arrest followed by 8 min of closed-chest CPR. During CPR, the animals were randomized to receive 60 mg/kg S-PBN, 1 mmol/kg TBM or 2 ml/kg normal saline (n = 10 in each group). Systemic haemodynamic variables, CCBF and jugular bulb plasma concentrations of 8-iso-PGF2alpha and 15-keto-dihydro-PGF2alpha were measured.RESULTS: The CCBF during reperfusion after ROSC was greater in the TBM group than in the S-PBN group, the regression coefficient between CCBF and mean arterial blood pressure being lower in the S-PBN group than in the TBM group. The jugular bulb plasma concentration of 8-iso-PGF2alpha during the first 30 min after ROSC was greater in the TBM group than in the S-PBN group. Administration of TBM after vasopressin did not attenuate the pressor effect of vasopressin.CONCLUSION: Administration of S-PBN during CPR results in less cerebral oxidative stress, possibly by promoting normal distribution of cerebral blood flow.
653 a CPR
653 a reperfusion injury
653 a oxidative damage
653 a free radical
653 a S-PBN
653 a cerebral haemodynamics
653 a vasopressin
653 a buffer
653 a MEDICINE
653 a MEDICIN
700a Wiklund, Larsu Uppsala universitet,Anestesiologi och intensivvård4 aut0 (Swepub:uu)larswikl
700a Nozari, A.u Uppsala universitet,Institutionen för kirurgiska vetenskaper,Anaesthesiology and Intensive Care4 aut
700a Rubertsson, Stenu Uppsala universitet,Anestesiologi och intensivvård4 aut0 (Swepub:uu)stenrube
700a Basu, Samaru Uppsala universitet,Institutionen för folkhälso- och vårdvetenskap,Clinical Nutrition4 aut
710a Uppsala universitetb Institutionen för kirurgiska vetenskaper4 org
773t Acta Anaesthesiologica Scandinavicad : Wileyg 47:8, s. 958-967q 47:8<958-967x 0001-5172x 1399-6576
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-65047
8564 8u https://doi.org/10.1034/j.1399-6576.2003.00189.x

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