Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion?
Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triio...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Pantos, Constantinos [verfasserIn] Mourouzis, Iordanis [verfasserIn] Saranteas, Theodosios [verfasserIn] Clavé, Guillaume [verfasserIn] Ligeret, Heidi [verfasserIn] Noack-Fraissignes, Pauline [verfasserIn] Renard, Pierre-Yves [verfasserIn] Massonneau, Marc [verfasserIn] Perimenis, Philipos [verfasserIn] Spanou, Danai [verfasserIn] Kostopanagiotou, Georgia [verfasserIn] Cokkinos, Dennis V. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Basic research in cardiology - [Darmstadt u.a.] : Steinkopff, 1937, 104(2009), 1 vom: Jan., Seite 69-77 |
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| Übergeordnetes Werk: |
volume:104 ; year:2009 ; number:1 ; month:01 ; pages:69-77 |
| Links: |
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| DOI / URN: |
10.1007/s00395-008-0758-4 |
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| Katalog-ID: |
SPR004889983 |
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| 100 | 1 | |a Pantos, Constantinos |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
| 264 | 1 | |c 2009 | |
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| 337 | |a Computermedien |b c |2 rdamedia | ||
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| 520 | |a Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. | ||
| 650 | 4 | |a thyroxine |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a inotropes |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ischaemia-reperfusion |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a apoptosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a MAPKs |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a myocardial infarction |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a caspase-3 |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Mourouzis, Iordanis |e verfasserin |4 aut | |
| 700 | 1 | |a Saranteas, Theodosios |e verfasserin |4 aut | |
| 700 | 1 | |a Clavé, Guillaume |e verfasserin |4 aut | |
| 700 | 1 | |a Ligeret, Heidi |e verfasserin |4 aut | |
| 700 | 1 | |a Noack-Fraissignes, Pauline |e verfasserin |4 aut | |
| 700 | 1 | |a Renard, Pierre-Yves |e verfasserin |4 aut | |
| 700 | 1 | |a Massonneau, Marc |e verfasserin |4 aut | |
| 700 | 1 | |a Perimenis, Philipos |e verfasserin |4 aut | |
| 700 | 1 | |a Spanou, Danai |e verfasserin |4 aut | |
| 700 | 1 | |a Kostopanagiotou, Georgia |e verfasserin |4 aut | |
| 700 | 1 | |a Cokkinos, Dennis V. |e verfasserin |4 aut | |
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10.1007/s00395-008-0758-4 doi (DE-627)SPR004889983 (SPR)s00395-008-0758-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Pantos, Constantinos verfasserin aut Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. thyroxine (dpeaa)DE-He213 inotropes (dpeaa)DE-He213 ischaemia-reperfusion (dpeaa)DE-He213 apoptosis (dpeaa)DE-He213 MAPKs (dpeaa)DE-He213 myocardial infarction (dpeaa)DE-He213 caspase-3 (dpeaa)DE-He213 Mourouzis, Iordanis verfasserin aut Saranteas, Theodosios verfasserin aut Clavé, Guillaume verfasserin aut Ligeret, Heidi verfasserin aut Noack-Fraissignes, Pauline verfasserin aut Renard, Pierre-Yves verfasserin aut Massonneau, Marc verfasserin aut Perimenis, Philipos verfasserin aut Spanou, Danai verfasserin aut Kostopanagiotou, Georgia verfasserin aut Cokkinos, Dennis V. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 104(2009), 1 vom: Jan., Seite 69-77 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:104 year:2009 number:1 month:01 pages:69-77 https://dx.doi.org/10.1007/s00395-008-0758-4 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_152 GBV_ILN_161 GBV_ILN_165 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_711 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_4277 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 44.85 ASE AR 104 2009 1 01 69-77 |
| spelling |
10.1007/s00395-008-0758-4 doi (DE-627)SPR004889983 (SPR)s00395-008-0758-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Pantos, Constantinos verfasserin aut Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. thyroxine (dpeaa)DE-He213 inotropes (dpeaa)DE-He213 ischaemia-reperfusion (dpeaa)DE-He213 apoptosis (dpeaa)DE-He213 MAPKs (dpeaa)DE-He213 myocardial infarction (dpeaa)DE-He213 caspase-3 (dpeaa)DE-He213 Mourouzis, Iordanis verfasserin aut Saranteas, Theodosios verfasserin aut Clavé, Guillaume verfasserin aut Ligeret, Heidi verfasserin aut Noack-Fraissignes, Pauline verfasserin aut Renard, Pierre-Yves verfasserin aut Massonneau, Marc verfasserin aut Perimenis, Philipos verfasserin aut Spanou, Danai verfasserin aut Kostopanagiotou, Georgia verfasserin aut Cokkinos, Dennis V. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 104(2009), 1 vom: Jan., Seite 69-77 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:104 year:2009 number:1 month:01 pages:69-77 https://dx.doi.org/10.1007/s00395-008-0758-4 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_152 GBV_ILN_161 GBV_ILN_165 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_711 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_4277 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 44.85 ASE AR 104 2009 1 01 69-77 |
| allfields_unstemmed |
10.1007/s00395-008-0758-4 doi (DE-627)SPR004889983 (SPR)s00395-008-0758-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Pantos, Constantinos verfasserin aut Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. thyroxine (dpeaa)DE-He213 inotropes (dpeaa)DE-He213 ischaemia-reperfusion (dpeaa)DE-He213 apoptosis (dpeaa)DE-He213 MAPKs (dpeaa)DE-He213 myocardial infarction (dpeaa)DE-He213 caspase-3 (dpeaa)DE-He213 Mourouzis, Iordanis verfasserin aut Saranteas, Theodosios verfasserin aut Clavé, Guillaume verfasserin aut Ligeret, Heidi verfasserin aut Noack-Fraissignes, Pauline verfasserin aut Renard, Pierre-Yves verfasserin aut Massonneau, Marc verfasserin aut Perimenis, Philipos verfasserin aut Spanou, Danai verfasserin aut Kostopanagiotou, Georgia verfasserin aut Cokkinos, Dennis V. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 104(2009), 1 vom: Jan., Seite 69-77 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:104 year:2009 number:1 month:01 pages:69-77 https://dx.doi.org/10.1007/s00395-008-0758-4 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_152 GBV_ILN_161 GBV_ILN_165 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_711 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_4277 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 44.85 ASE AR 104 2009 1 01 69-77 |
| allfieldsGer |
10.1007/s00395-008-0758-4 doi (DE-627)SPR004889983 (SPR)s00395-008-0758-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Pantos, Constantinos verfasserin aut Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. thyroxine (dpeaa)DE-He213 inotropes (dpeaa)DE-He213 ischaemia-reperfusion (dpeaa)DE-He213 apoptosis (dpeaa)DE-He213 MAPKs (dpeaa)DE-He213 myocardial infarction (dpeaa)DE-He213 caspase-3 (dpeaa)DE-He213 Mourouzis, Iordanis verfasserin aut Saranteas, Theodosios verfasserin aut Clavé, Guillaume verfasserin aut Ligeret, Heidi verfasserin aut Noack-Fraissignes, Pauline verfasserin aut Renard, Pierre-Yves verfasserin aut Massonneau, Marc verfasserin aut Perimenis, Philipos verfasserin aut Spanou, Danai verfasserin aut Kostopanagiotou, Georgia verfasserin aut Cokkinos, Dennis V. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 104(2009), 1 vom: Jan., Seite 69-77 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:104 year:2009 number:1 month:01 pages:69-77 https://dx.doi.org/10.1007/s00395-008-0758-4 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_152 GBV_ILN_161 GBV_ILN_165 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_711 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_4277 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 44.85 ASE AR 104 2009 1 01 69-77 |
| allfieldsSound |
10.1007/s00395-008-0758-4 doi (DE-627)SPR004889983 (SPR)s00395-008-0758-4-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.85 bkl Pantos, Constantinos verfasserin aut Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. thyroxine (dpeaa)DE-He213 inotropes (dpeaa)DE-He213 ischaemia-reperfusion (dpeaa)DE-He213 apoptosis (dpeaa)DE-He213 MAPKs (dpeaa)DE-He213 myocardial infarction (dpeaa)DE-He213 caspase-3 (dpeaa)DE-He213 Mourouzis, Iordanis verfasserin aut Saranteas, Theodosios verfasserin aut Clavé, Guillaume verfasserin aut Ligeret, Heidi verfasserin aut Noack-Fraissignes, Pauline verfasserin aut Renard, Pierre-Yves verfasserin aut Massonneau, Marc verfasserin aut Perimenis, Philipos verfasserin aut Spanou, Danai verfasserin aut Kostopanagiotou, Georgia verfasserin aut Cokkinos, Dennis V. verfasserin aut Enthalten in Basic research in cardiology [Darmstadt u.a.] : Steinkopff, 1937 104(2009), 1 vom: Jan., Seite 69-77 (DE-627)253390265 (DE-600)1458470-0 1435-1803 nnns volume:104 year:2009 number:1 month:01 pages:69-77 https://dx.doi.org/10.1007/s00395-008-0758-4 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_152 GBV_ILN_161 GBV_ILN_165 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_711 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_4277 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 44.85 ASE AR 104 2009 1 01 69-77 |
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Enthalten in Basic research in cardiology 104(2009), 1 vom: Jan., Seite 69-77 volume:104 year:2009 number:1 month:01 pages:69-77 |
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thyroxine inotropes ischaemia-reperfusion apoptosis MAPKs myocardial infarction caspase-3 |
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Basic research in cardiology |
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Pantos, Constantinos @@aut@@ Mourouzis, Iordanis @@aut@@ Saranteas, Theodosios @@aut@@ Clavé, Guillaume @@aut@@ Ligeret, Heidi @@aut@@ Noack-Fraissignes, Pauline @@aut@@ Renard, Pierre-Yves @@aut@@ Massonneau, Marc @@aut@@ Perimenis, Philipos @@aut@@ Spanou, Danai @@aut@@ Kostopanagiotou, Georgia @@aut@@ Cokkinos, Dennis V. @@aut@@ |
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2009-01-01T00:00:00Z |
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| author |
Pantos, Constantinos |
| spellingShingle |
Pantos, Constantinos ddc 610 bkl 44.85 misc thyroxine misc inotropes misc ischaemia-reperfusion misc apoptosis misc MAPKs misc myocardial infarction misc caspase-3 Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
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610 ASE 44.85 bkl Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? thyroxine (dpeaa)DE-He213 inotropes (dpeaa)DE-He213 ischaemia-reperfusion (dpeaa)DE-He213 apoptosis (dpeaa)DE-He213 MAPKs (dpeaa)DE-He213 myocardial infarction (dpeaa)DE-He213 caspase-3 (dpeaa)DE-He213 |
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ddc 610 bkl 44.85 misc thyroxine misc inotropes misc ischaemia-reperfusion misc apoptosis misc MAPKs misc myocardial infarction misc caspase-3 |
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ddc 610 bkl 44.85 misc thyroxine misc inotropes misc ischaemia-reperfusion misc apoptosis misc MAPKs misc myocardial infarction misc caspase-3 |
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Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
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(DE-627)SPR004889983 (SPR)s00395-008-0758-4-e |
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Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
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Pantos, Constantinos |
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Basic research in cardiology |
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Pantos, Constantinos Mourouzis, Iordanis Saranteas, Theodosios Clavé, Guillaume Ligeret, Heidi Noack-Fraissignes, Pauline Renard, Pierre-Yves Massonneau, Marc Perimenis, Philipos Spanou, Danai Kostopanagiotou, Georgia Cokkinos, Dennis V. |
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Pantos, Constantinos |
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10.1007/s00395-008-0758-4 |
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610 |
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verfasserin |
| title_sort |
thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
| title_auth |
Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
| abstract |
Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. |
| abstractGer |
Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. |
| abstract_unstemmed |
Abstract Although it has long been recognized that thyroid hormone is an effective positive inotrope, its efficacy in supporting hemodynamics in the acute setting of ischaemia and reperfusion (R) without worsening reperfusion injury remains largely unknown. Thus, we investigated the effects of triiodothyronine (T3) on reperfusion injury in a Langendorff–perfused rat heart model of 30 min zero-flow ischaemia and 60 min of (R) with or without T3 (40 µg/l) at R, T3-R60, n = 11 and CNT-R60, n = 10, respectively. Furthermore, phosphorylated levels of intracellular kinases were measured at 5, 15 and 60 min of R. T3 markedly improved postischaemic recovery of left ventricular developed pressure (LVDP%); 56.0% (SEM, 4.4) in T3-R60 versus 38.8% (3.1) in CNT-R60, P < 0.05. Furthermore, LDH release was significantly lower in T3-R60. Apoptosis detection by fluorescent probe optical imaging showed increased fluorescent signal in CNT-R60 hearts, while the signal was hardly detectable in T3-R60 hearts. Similarly, caspase-3 activity was found to be 78.2 (8.2) in CNT-R60 vs 40.5 (7.1) in T3-R60 hearts, P < 0.05. This response was associated with significantly lower levels of phospho-p38 MAPK at any time point of R. No significant changes in phospho- ERK1/2 and JNK levels were observed between groups. Phospho–Akt levels were significantly lower in T3 treated group at 5 min and no change in phospho–Akt levels were observed at 15 and 60 min between groups. In conclusion, T3 administration at reperfusion can improve postischaemic recovery of function while limiting apoptosis. This may constitute a paradigm of a positive inotropic agent with anti-apoptotic action suitable for supporting hemodynamics in the clinical setting of ischaemia-reperfusion. |
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Thyroid hormone improves postischaemic recovery of function while limiting apoptosis: a new therapeutic approach to support hemodynamics in the setting of ischaemia-reperfusion? |
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https://dx.doi.org/10.1007/s00395-008-0758-4 |
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Mourouzis, Iordanis Saranteas, Theodosios Clavé, Guillaume Ligeret, Heidi Noack-Fraissignes, Pauline Renard, Pierre-Yves Massonneau, Marc Perimenis, Philipos Spanou, Danai Kostopanagiotou, Georgia Cokkinos, Dennis V. |
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Mourouzis, Iordanis Saranteas, Theodosios Clavé, Guillaume Ligeret, Heidi Noack-Fraissignes, Pauline Renard, Pierre-Yves Massonneau, Marc Perimenis, Philipos Spanou, Danai Kostopanagiotou, Georgia Cokkinos, Dennis V. |
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10.1007/s00395-008-0758-4 |
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2024-07-04T02:56:00.315Z |
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| score |
7.4004908 |