Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle
Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of...
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Englisch |
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1999 |
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7 |
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Springer Online Journal Archives 1860-2002 |
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in: European journal of clinical pharmacology - 1968, 55(1999) vom: Jan., Seite 35-41 |
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volume:55 ; year:1999 ; month:01 ; pages:35-41 ; extent:7 |
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| 520 | |a Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. | ||
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| 700 | 1 | |a Alonso, J. R. |4 oth | |
| 700 | 1 | |a Casademont, J. |4 oth | |
| 700 | 1 | |a Jarreta, D. |4 oth | |
| 700 | 1 | |a Urbano-Márquez, Á. |4 oth | |
| 700 | 1 | |a Cardellach, F. |4 oth | |
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(DE-627)NLEJ202480054 DE-627 ger DE-627 rakwb eng Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle 1999 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. Springer Online Journal Archives 1860-2002 Miró, Ò. oth Barrientos, A. oth Alonso, J. R. oth Casademont, J. oth Jarreta, D. oth Urbano-Márquez, Á. oth Cardellach, F. oth in European journal of clinical pharmacology 1968 55(1999) vom: Jan., Seite 35-41 (DE-627)NLEJ188986677 (DE-600)1459058-x 1432-1041 nnns volume:55 year:1999 month:01 pages:35-41 extent:7 http://dx.doi.org/10.1007/s002280050589 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 55 1999 1 35-41 7 |
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(DE-627)NLEJ202480054 DE-627 ger DE-627 rakwb eng Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle 1999 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. Springer Online Journal Archives 1860-2002 Miró, Ò. oth Barrientos, A. oth Alonso, J. R. oth Casademont, J. oth Jarreta, D. oth Urbano-Márquez, Á. oth Cardellach, F. oth in European journal of clinical pharmacology 1968 55(1999) vom: Jan., Seite 35-41 (DE-627)NLEJ188986677 (DE-600)1459058-x 1432-1041 nnns volume:55 year:1999 month:01 pages:35-41 extent:7 http://dx.doi.org/10.1007/s002280050589 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 55 1999 1 35-41 7 |
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(DE-627)NLEJ202480054 DE-627 ger DE-627 rakwb eng Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle 1999 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. Springer Online Journal Archives 1860-2002 Miró, Ò. oth Barrientos, A. oth Alonso, J. R. oth Casademont, J. oth Jarreta, D. oth Urbano-Márquez, Á. oth Cardellach, F. oth in European journal of clinical pharmacology 1968 55(1999) vom: Jan., Seite 35-41 (DE-627)NLEJ188986677 (DE-600)1459058-x 1432-1041 nnns volume:55 year:1999 month:01 pages:35-41 extent:7 http://dx.doi.org/10.1007/s002280050589 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 55 1999 1 35-41 7 |
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(DE-627)NLEJ202480054 DE-627 ger DE-627 rakwb eng Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle 1999 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. Springer Online Journal Archives 1860-2002 Miró, Ò. oth Barrientos, A. oth Alonso, J. R. oth Casademont, J. oth Jarreta, D. oth Urbano-Márquez, Á. oth Cardellach, F. oth in European journal of clinical pharmacology 1968 55(1999) vom: Jan., Seite 35-41 (DE-627)NLEJ188986677 (DE-600)1459058-x 1432-1041 nnns volume:55 year:1999 month:01 pages:35-41 extent:7 http://dx.doi.org/10.1007/s002280050589 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 55 1999 1 35-41 7 |
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Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. |
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Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. |
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Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ202480054</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506153004.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1999 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ202480054</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="245" ind1="1" ind2="0"><subfield code="a">Effects of general anaesthetic procedures on mitochondrial function of human skeletal muscle</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1999</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Background: General anaesthetics inhibit mitochondrial function in animal models. However, very few studies have been performed in humans, and the results have not been conclusive. Methods: We prospectively studied the oxygen consumption and the individual enzyme activity of each complex of the mitochondrial respiratory chain of skeletal muscle mitochondria in 54 healthy individuals who underwent general anaesthesia for orthopaedic surgery. The control group (n = 54) was made up of individuals submitted to the same orthopaedic procedure under regional anaesthesia (n = 31), and patients who underwent muscle biopsies for diagnostic purposes by local anaesthesia (n = 23). Results: We found a significant decrease in the oxidation of glutamate (−36%), succinate (−25%) and ascorbate (−29%) in the general anaesthetic group compared with the controls (P < 0.001 for all substrates). The level of such inhibition was similar for volatile anaesthetics with strong (halothane) or weak (isoflurane) negative inotropic effect. By contrast, the enzymatic activity of all individual complexes and the coupling of oxidative phosphorylation did not differ between the two groups. Conclusion: We conclude that during general anaesthetic procedures there is an extensive inhibition of substrate oxidation in human muscle mitochondria, and that it is not caused by a direct effect on complexes of the mitochondrial respiratory chain or through uncoupling oxidative phosphorylation.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Miró, Ò.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Barrientos, A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Alonso, J. R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Casademont, J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jarreta, D.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Urbano-Márquez, Á.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cardellach, F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">European journal of clinical pharmacology</subfield><subfield code="d">1968</subfield><subfield code="g">55(1999) vom: Jan., Seite 35-41</subfield><subfield code="w">(DE-627)NLEJ188986677</subfield><subfield code="w">(DE-600)1459058-x</subfield><subfield code="x">1432-1041</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:55</subfield><subfield code="g">year:1999</subfield><subfield code="g">month:01</subfield><subfield code="g">pages:35-41</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/s002280050589</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">55</subfield><subfield code="j">1999</subfield><subfield code="c">1</subfield><subfield code="h">35-41</subfield><subfield code="g">7</subfield></datafield></record></collection>
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