Interleukin-6 Causes Myocardial Failure and Skeletal Muscle Atrophy in Rats
Background— The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. Methods and Results— The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 μg · kg −1 · d −1 , in rats. Skeletal muscle mass dec...
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| Published in | Circulation (New York, N.Y.) Vol. 111; no. 8; pp. 996 - 1005 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
01.03.2005
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background—
The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy.
Methods and Results—
The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 μg · kg
−1
· d
−1
, in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, −10%,
P
=NS; −15%,
P
=0.0561; and −15%
P
<0.05; and in the gastrocnemius, −9%,
P
=NS; −9%,
P
=NS; and −18%,
P
<0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 μL; moderate dose, 123 μL; and high dose, 137 μL,
P
<0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg;
P
=0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg;
P
<0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5;
P
<0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL · min
−1
· g
−1
; moderate dose, 0.21 mL · min
−1
· g
−1
; and high dose, 0.23 mL · min
−1
· g
−1
;
P
=0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity.
Conclusions—
IL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm. |
|---|---|
| AbstractList | BACKGROUND: The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. METHOD:S: and Results-The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 kg . kg super(-1) . d super(-1), in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, -10%, P=NS; -15%, P=0.0561; and -15% P<0.05; and in the gastrocnemius, -9%, P=NS; -9%, P=NS; and -18%, P<0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 kL; moderate dose, 123 kL; and high dose, 137 kL, P<0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; P=0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; P<0.001). Lung edema was confirmed by an increased wet-to- dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; P<0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL . min super(-1) . g super(- 1); moderate dose, 0.21 mL . min super(-1) . g super(-1); and high dose, 0.23 mL . min super(-1) . g super(-1); P=0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity. CONCLUSIONS: IL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm. The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy.BACKGROUNDThe impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy.The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 microg x kg(-1) x d(-1), in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, -10%, P=NS; -15%, P=0.0561; and -15% P<0.05; and in the gastrocnemius, -9%, P=NS; -9%, P=NS; and -18%, P<0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 microL; moderate dose, 123 microL; and high dose, 137 microL, P<0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; P=0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; P<0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; P<0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL x min(-1) x g(-1); moderate dose, 0.21 mL x min(-1) x g(-1); and high dose, 0.23 mL x min(-1) x g(-1); P=0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity.METHODS AND RESULTSThe effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 microg x kg(-1) x d(-1), in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, -10%, P=NS; -15%, P=0.0561; and -15% P<0.05; and in the gastrocnemius, -9%, P=NS; -9%, P=NS; and -18%, P<0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 microL; moderate dose, 123 microL; and high dose, 137 microL, P<0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; P=0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; P<0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; P<0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL x min(-1) x g(-1); moderate dose, 0.21 mL x min(-1) x g(-1); and high dose, 0.23 mL x min(-1) x g(-1); P=0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity.IL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm.CONCLUSIONSIL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm. The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 microg x kg(-1) x d(-1), in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, -10%, P=NS; -15%, P=0.0561; and -15% P<0.05; and in the gastrocnemius, -9%, P=NS; -9%, P=NS; and -18%, P<0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 microL; moderate dose, 123 microL; and high dose, 137 microL, P<0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; P=0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; P<0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; P<0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL x min(-1) x g(-1); moderate dose, 0.21 mL x min(-1) x g(-1); and high dose, 0.23 mL x min(-1) x g(-1); P=0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity. IL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm. Background— The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. Methods and Results— The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 μg · kg −1 · d −1 , in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, −10%, P =NS; −15%, P =0.0561; and −15% P <0.05; and in the gastrocnemius, −9%, P =NS; −9%, P =NS; and −18%, P <0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 μL; moderate dose, 123 μL; and high dose, 137 μL, P <0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; P =0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; P <0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; P <0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL · min −1 · g −1 ; moderate dose, 0.21 mL · min −1 · g −1 ; and high dose, 0.23 mL · min −1 · g −1 ; P =0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity. Conclusions— IL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm. |
| Author | Van Den Bergh, An Decramer, Marc Janssen, Sofie P.M. Herijgers, Paul Verbeken, Erik Gayan-Ramirez, Ghislaine Maes, Karen |
| Author_xml | – sequence: 1 givenname: Sofie P.M. surname: Janssen fullname: Janssen, Sofie P.M. organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium – sequence: 2 givenname: Ghislaine surname: Gayan-Ramirez fullname: Gayan-Ramirez, Ghislaine organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium – sequence: 3 givenname: An surname: Van Den Bergh fullname: Van Den Bergh, An organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium – sequence: 4 givenname: Paul surname: Herijgers fullname: Herijgers, Paul organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium – sequence: 5 givenname: Karen surname: Maes fullname: Maes, Karen organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium – sequence: 6 givenname: Erik surname: Verbeken fullname: Verbeken, Erik organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium – sequence: 7 givenname: Marc surname: Decramer fullname: Decramer, Marc organization: From the Laboratory of Pneumology (S.P.M.J., G.G.-R., K.M., M.D.), Respiratory Muscle Research Unit; the Center for Experimental Surgery and Anesthesiology (A.V.D.B., P.H.), Cardiovascular Research Unit; and the Department of Pathology (E.V.), Katholieke Universiteit Leuven, Leuven, Belgium |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16585827$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/15710765$$D View this record in MEDLINE/PubMed |
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| Issue | 8 |
| Keywords | Rat Cardiomyopathy Cytokine Rodentia Contractility Cardiovascular disease Striated muscle Myocardial disease Blood flow interleukins Atrophy Interleukin 6 Vertebrata Mammalia muscles Heart disease Animal Hemodynamics |
| Language | English |
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| PublicationTitle | Circulation (New York, N.Y.) |
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| Snippet | Background—
The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy.
Methods and Results—
The effects of 7-day... The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. The effects of 7-day subcutaneous administration of... The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy.BACKGROUNDThe impact of interleukin (IL)-6 on skeletal muscle... BACKGROUND: The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. METHOD:S: and Results-The effects of 7-day... |
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| SubjectTerms | Animals Antihypertensive agents Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Body Weight - drug effects Cardiology. Vascular system Cardiomyopathies - chemically induced Cardiovascular system Cardiovascular System - drug effects Cardiovascular System - physiopathology Coronary Vessels - drug effects Coronary Vessels - physiopathology Diaphragm - blood supply Diaphragm - metabolism Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Dose-Response Relationship, Drug Eating - drug effects Eating - physiology Fundamental and applied biological sciences. Psychology Heart Failure - chemically induced In Vitro Techniques Interleukin-6 - administration & dosage Interleukin-6 - blood Interleukin-6 - pharmacology Liver - blood supply Liver - metabolism Lung - blood supply Lung - metabolism Male Medical sciences Motor Activity - drug effects Motor Activity - physiology Muscle Contraction - drug effects Muscle Contraction - physiology Muscle, Skeletal - blood supply Muscle, Skeletal - drug effects Muscle, Skeletal - physiopathology Muscular Atrophy - chemically induced Myocardial Contraction - drug effects Myocardial Contraction - physiology Myocardium - pathology Organ Size - drug effects Pharmacology. Drug treatments Rats Rats, Wistar Recombinant Proteins - administration & dosage Regional Blood Flow - drug effects Regional Blood Flow - physiology Vertebrates: cardiovascular system |
| Title | Interleukin-6 Causes Myocardial Failure and Skeletal Muscle Atrophy in Rats |
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