Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia

Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain d...
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Autor*in:	Lehmberg, J. [verfasserIn] Beck, J. [verfasserIn] Baethmann, A. [verfasserIn] Uhl, E. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2005

Übergeordnetes Werk:	Enthalten in: Journal of neurology - [Darmstadt] : Steinkopff, 1891, 253(2005), 3 vom: 10. Okt., Seite 357-363
Übergeordnetes Werk:	volume:253 ; year:2005 ; number:3 ; day:10 ; month:10 ; pages:357-363

Links:	Volltext

DOI / URN:	10.1007/s00415-005-0996-4

Katalog-ID:	SPR005321255

Internformat


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245	1	0	\|a Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
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520			\|a Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia.
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912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2070
912			\|a GBV_ILN_2086
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2093
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author_variant	j l jl j b jb a b ab e u eu
matchkey_str	article:14321459:2005----::fetfslciihbtooluoyenohluitrcinnsriaa
hierarchy_sort_str	2005
bklnumber	44.90
publishDate	2005
allfields	10.1007/s00415-005-0996-4 doi (DE-627)SPR005321255 (SPR)s00415-005-0996-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lehmberg, J. verfasserin aut Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia. Beck, J. verfasserin aut Baethmann, A. verfasserin aut Uhl, E. verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 253(2005), 3 vom: 10. Okt., Seite 357-363 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:253 year:2005 number:3 day:10 month:10 pages:357-363 https://dx.doi.org/10.1007/s00415-005-0996-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_724 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 253 2005 3 10 10 357-363
spelling	10.1007/s00415-005-0996-4 doi (DE-627)SPR005321255 (SPR)s00415-005-0996-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lehmberg, J. verfasserin aut Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia. Beck, J. verfasserin aut Baethmann, A. verfasserin aut Uhl, E. verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 253(2005), 3 vom: 10. Okt., Seite 357-363 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:253 year:2005 number:3 day:10 month:10 pages:357-363 https://dx.doi.org/10.1007/s00415-005-0996-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_724 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 253 2005 3 10 10 357-363
allfields_unstemmed	10.1007/s00415-005-0996-4 doi (DE-627)SPR005321255 (SPR)s00415-005-0996-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lehmberg, J. verfasserin aut Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia. Beck, J. verfasserin aut Baethmann, A. verfasserin aut Uhl, E. verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 253(2005), 3 vom: 10. Okt., Seite 357-363 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:253 year:2005 number:3 day:10 month:10 pages:357-363 https://dx.doi.org/10.1007/s00415-005-0996-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_724 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 253 2005 3 10 10 357-363
allfieldsGer	10.1007/s00415-005-0996-4 doi (DE-627)SPR005321255 (SPR)s00415-005-0996-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lehmberg, J. verfasserin aut Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia. Beck, J. verfasserin aut Baethmann, A. verfasserin aut Uhl, E. verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 253(2005), 3 vom: 10. Okt., Seite 357-363 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:253 year:2005 number:3 day:10 month:10 pages:357-363 https://dx.doi.org/10.1007/s00415-005-0996-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_724 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 253 2005 3 10 10 357-363
allfieldsSound	10.1007/s00415-005-0996-4 doi (DE-627)SPR005321255 (SPR)s00415-005-0996-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lehmberg, J. verfasserin aut Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia. Beck, J. verfasserin aut Baethmann, A. verfasserin aut Uhl, E. verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 253(2005), 3 vom: 10. Okt., Seite 357-363 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:253 year:2005 number:3 day:10 month:10 pages:357-363 https://dx.doi.org/10.1007/s00415-005-0996-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_724 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 253 2005 3 10 10 357-363
language	English
source	Enthalten in Journal of neurology 253(2005), 3 vom: 10. Okt., Seite 357-363 volume:253 year:2005 number:3 day:10 month:10 pages:357-363
sourceStr	Enthalten in Journal of neurology 253(2005), 3 vom: 10. Okt., Seite 357-363 volume:253 year:2005 number:3 day:10 month:10 pages:357-363
format_phy_str_mv	Article
institution	findex.gbv.de
dewey-raw	610
isfreeaccess_bool	false
container_title	Journal of neurology
authorswithroles_txt_mv	Lehmberg, J. @@aut@@ Beck, J. @@aut@@ Baethmann, A. @@aut@@ Uhl, E. @@aut@@
publishDateDaySort_date	2005-10-10T00:00:00Z
hierarchy_top_id	242065155
dewey-sort	3610
id	SPR005321255
language_de	englisch
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author	Lehmberg, J.
spellingShingle	Lehmberg, J. ddc 610 bkl 44.90 Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
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topic_title	610 ASE 44.90 bkl Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
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title	Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
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title_full	Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
author_sort	Lehmberg, J.
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author_browse	Lehmberg, J. Beck, J. Baethmann, A. Uhl, E.
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title_sort	effect of p–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
title_auth	Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
abstract	Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia.
abstractGer	Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia.
abstract_unstemmed	Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia.
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title_short	Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia
url	https://dx.doi.org/10.1007/s00415-005-0996-4
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author2	Beck, J. Baethmann, A. Uhl, E.
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doi_str	10.1007/s00415-005-0996-4
up_date	2024-07-03T15:31:21.211Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR005321255</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519225207.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201001s2005 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00415-005-0996-4</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR005321255</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00415-005-0996-4-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Lehmberg, J.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2005</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Cerebral ischemiainduces activation of leukocyteendotheliuminteractions requiringupregulation of specific adhesionmolecules including the selectins.The aim of the current study was toelucidate the therapeutic potencyof P–selectin blockade on microcirculatorydisturbances and secondarybrain damage after globalcerebral ischemia. Global cerebralischemia for 15 minutes was inducedin Mongolian gerbils. Functionalblockade of P–selectin wasachieved by pretreatment with theantibody RB 40.34 (2 mg/kg, n = 7).In vivo observation of brain microcirculationwas performed by epifluorescencemicroscopy of a cranialwindow. Survival was assesseddaily up to 4 days after ischemia.In the control group leukocyterolling increased during reperfusionwith a maximum at 3 h(28 ± 14 · $ 100μm^{–1} $ · $ min^{–1} $)and was significantly reducedby the P–selectin antibody(13 ± 9 ·$ 100μm^{–1} $ ·$ min^{–1} $,p <0.05).No effect on firm leukocyte adhesionwas observed (4 ± 3 vs.2 ± 1 · $ 100μm^{–1} $ · $ min^{–1} $). The survivalof animals that received the Pselectinantibody (28 %) was significantlyreduced compared withcontrols (71 %). Anti–P–selectin antibodyreduces leukocyte rollingbut has no positive effect on survival.Our data question the role ofthe inflammatory response in thedevelopment of secondary braindamage and do not support thiskind of therapeutical approach inglobal cerebral ischemia.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Beck, J.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Baethmann, A.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Uhl, E.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of neurology</subfield><subfield code="d">[Darmstadt] : Steinkopff, 1891</subfield><subfield code="g">253(2005), 3 vom: 10. 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Effect of P–selectin inhibition on leukocyteendothelium interaction and survival after global cerebral ischemia

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