The carbon monoxide prodrug oCOm‐21 increases Ca2+ sensitivity of the cardiac myofilament
Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca2+ flux. Low‐dose carbon...
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| Published in | Physiological reports Vol. 12; no. 6; pp. e15974 - n/a |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
John Wiley & Sons, Inc
01.03.2024
John Wiley and Sons Inc Wiley |
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| Abstract | Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca2+ flux. Low‐dose carbon monoxide (CO) induces inotropic effects in perfused hearts. Using the CO‐releasing pro‐drug, oCOm‐21, we investigated if this inotropic effect results from an increase in myofilament Ca2+ sensitivity. Male Sprague Dawley rat left ventricular cardiomyocytes were permeabilized, and myofilament force was measured as a function of ‐log [Ca2+] (pCa) in the range of 9.0–4.5 under five conditions: vehicle, oCOm‐21, the oCOm‐21 control BP‐21, and levosimendan, (9 cells/group). Ca2+ sensitivity was assessed by the Ca2+ concentration at which 50% of maximal force is produced (pCa50). oCOm‐21, but not BP‐21 significantly increased pCa50 compared to vehicle, respectively (pCa50 5.52 vs. 5.47 vs. 5.44; p < 0.05). No change in myofilament phosphorylation was seen after oCOm‐21 treatment. Pretreatment of cardiomyocytes with the heme scavenger hemopexin, abolished the Ca2+ sensitizing effect of oCOm‐21. These results support the hypothesis that oCOm‐21‐derived CO increases myofilament Ca2+ sensitivity through a heme‐dependent mechanism but not by phosphorylation. Further analyses will confirm if this Ca2+ sensitizing effect occurs in an intact heart. |
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| AbstractList | Abstract Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca2+ flux. Low‐dose carbon monoxide (CO) induces inotropic effects in perfused hearts. Using the CO‐releasing pro‐drug, oCOm‐21, we investigated if this inotropic effect results from an increase in myofilament Ca2+ sensitivity. Male Sprague Dawley rat left ventricular cardiomyocytes were permeabilized, and myofilament force was measured as a function of ‐log [Ca2+] (pCa) in the range of 9.0–4.5 under five conditions: vehicle, oCOm‐21, the oCOm‐21 control BP‐21, and levosimendan, (9 cells/group). Ca2+ sensitivity was assessed by the Ca2+ concentration at which 50% of maximal force is produced (pCa50). oCOm‐21, but not BP‐21 significantly increased pCa50 compared to vehicle, respectively (pCa50 5.52 vs. 5.47 vs. 5.44; p < 0.05). No change in myofilament phosphorylation was seen after oCOm‐21 treatment. Pretreatment of cardiomyocytes with the heme scavenger hemopexin, abolished the Ca2+ sensitizing effect of oCOm‐21. These results support the hypothesis that oCOm‐21‐derived CO increases myofilament Ca2+ sensitivity through a heme‐dependent mechanism but not by phosphorylation. Further analyses will confirm if this Ca2+ sensitizing effect occurs in an intact heart. Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca2+ flux. Low-dose carbon monoxide (CO) induces inotropic effects in perfused hearts. Using the CO-releasing pro-drug, oCOm-21, we investigated if this inotropic effect results from an increase in myofilament Ca2+ sensitivity. Male Sprague Dawley rat left ventricular cardiomyocytes were permeabilized, and myofilament force was measured as a function of -log [Ca2+] (pCa) in the range of 9.0–4.5 under five conditions: vehicle, oCOm-21, the oCOm-21 control BP-21, and levosimendan, (9 cells/group). Ca2+ sensitivity was assessed by the Ca2+ concentration at which 50% of maximal force is produced (pCa50). oCOm-21, but not BP-21 significantly increased pCa50 compared to vehicle, respectively (pCa50 5.52 vs. 5.47 vs. 5.44; p < 0.05). No change in myofilament phosphorylation was seen after oCOm-21 treatment. Pretreatment of cardiomyocytes with the heme scavenger hemopexin, abolished the Ca2+ sensitizing effect of oCOm-21. These results support the hypothesis that oCOm-21-derived CO increases myofilament Ca2+ sensitivity through a heme-dependent mechanism but not by phosphorylation. Further analyses will confirm if this Ca2+ sensitizing effect occurs in an intact heart. Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca2+ flux. Low-dose carbon monoxide (CO) induces inotropic effects in perfused hearts. Using the CO-releasing pro-drug, oCOm-21, we investigated if this inotropic effect results from an increase in myofilament Ca2+ sensitivity. Male Sprague Dawley rat left ventricular cardiomyocytes were permeabilized, and myofilament force was measured as a function of -log [Ca2+ ] (pCa) in the range of 9.0-4.5 under five conditions: vehicle, oCOm-21, the oCOm-21 control BP-21, and levosimendan, (9 cells/group). Ca2+ sensitivity was assessed by the Ca2+ concentration at which 50% of maximal force is produced (pCa50 ). oCOm-21, but not BP-21 significantly increased pCa50 compared to vehicle, respectively (pCa50 5.52 vs. 5.47 vs. 5.44; p < 0.05). No change in myofilament phosphorylation was seen after oCOm-21 treatment. Pretreatment of cardiomyocytes with the heme scavenger hemopexin, abolished the Ca2+ sensitizing effect of oCOm-21. These results support the hypothesis that oCOm-21-derived CO increases myofilament Ca2+ sensitivity through a heme-dependent mechanism but not by phosphorylation. Further analyses will confirm if this Ca2+ sensitizing effect occurs in an intact heart.Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca2+ flux. Low-dose carbon monoxide (CO) induces inotropic effects in perfused hearts. Using the CO-releasing pro-drug, oCOm-21, we investigated if this inotropic effect results from an increase in myofilament Ca2+ sensitivity. Male Sprague Dawley rat left ventricular cardiomyocytes were permeabilized, and myofilament force was measured as a function of -log [Ca2+ ] (pCa) in the range of 9.0-4.5 under five conditions: vehicle, oCOm-21, the oCOm-21 control BP-21, and levosimendan, (9 cells/group). Ca2+ sensitivity was assessed by the Ca2+ concentration at which 50% of maximal force is produced (pCa50 ). oCOm-21, but not BP-21 significantly increased pCa50 compared to vehicle, respectively (pCa50 5.52 vs. 5.47 vs. 5.44; p < 0.05). No change in myofilament phosphorylation was seen after oCOm-21 treatment. Pretreatment of cardiomyocytes with the heme scavenger hemopexin, abolished the Ca2+ sensitizing effect of oCOm-21. These results support the hypothesis that oCOm-21-derived CO increases myofilament Ca2+ sensitivity through a heme-dependent mechanism but not by phosphorylation. Further analyses will confirm if this Ca2+ sensitizing effect occurs in an intact heart. Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as dobutamine, can promote arrhythmias, prompting a demand for improved inotropes with little effect on intracellular Ca 2+ flux. Low‐dose carbon monoxide (CO) induces inotropic effects in perfused hearts. Using the CO‐releasing pro‐drug, oCOm‐21, we investigated if this inotropic effect results from an increase in myofilament Ca 2+ sensitivity. Male Sprague Dawley rat left ventricular cardiomyocytes were permeabilized, and myofilament force was measured as a function of ‐log [Ca 2+ ] (pCa) in the range of 9.0–4.5 under five conditions: vehicle, oCOm‐21, the oCOm‐21 control BP‐21, and levosimendan, (9 cells/group). Ca 2+ sensitivity was assessed by the Ca 2+ concentration at which 50% of maximal force is produced (pCa 50 ). oCOm‐21, but not BP‐21 significantly increased pCa 50 compared to vehicle, respectively (pCa 50 5.52 vs. 5.47 vs. 5.44; p < 0.05). No change in myofilament phosphorylation was seen after oCOm‐21 treatment. Pretreatment of cardiomyocytes with the heme scavenger hemopexin, abolished the Ca 2+ sensitizing effect of oCOm‐21. These results support the hypothesis that oCOm‐21‐derived CO increases myofilament Ca 2+ sensitivity through a heme‐dependent mechanism but not by phosphorylation. Further analyses will confirm if this Ca 2+ sensitizing effect occurs in an intact heart. |
| Author | Diffee, Gary M. Payne, Fergus M. Wilkins, Gerard T. Baldi, James C. Nie, Samantha Sammut, Ivan A. Harrison, Joanne C. Larsen, David S. |
| AuthorAffiliation | 4 Department of Kinesiology University of Wisconsin‐Madison Madison Wisconsin USA 3 HeartOtago University of Otago Dunedin New Zealand 5 School of Science, Department of Chemistry University of Otago Dunedin Otago New Zealand 2 Otago Medical School, Department of Medicine University of Otago Dunedin Otago New Zealand 1 School of Biomedical Sciences, Department of Pharmacology and Toxicology University of Otago Dunedin Otago New Zealand |
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| Copyright | 2024 The Authors. published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society. 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2024 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society. |
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| References | 2001; 91 2004; 486 2010; 99 2022; 132 2017; 8 2000; 6 2015; 467 2021; 402 1991; 97 1995; 77 2020; 17 2003; 57 2008; 108 1971; 245 1997; 280 2020; 10 2014; 171 2015; 89 1976; 73 2015; 172 2020; 1 1995; 27 2007; 292 2021; 116 2023; 299 2002; 540 2020; 9 1994; 33 2023; 214 1998; 125 2011; 162 2023; 14 2019; 73 1993; 306 2021; 106 2015; 10 2007; 92 2020; 34 1994; 81 1985; 260 2000; 192 1994; 9 2021; 14 2018; 18 2021; 10 2005; 19 2012; 111 2000; 39 2021; 134 2000; 78 1999; 274 2022; 12 2021; 173 2022; 15 1992; 24 2006; 149 2017; 389 2008; 295 2001; 158 |
| References_xml | – volume: 73 start-page: 2345 year: 2019 end-page: 2353 article-title: Cardiac calcitropes, myotropes, and mitotropes: JACC review topic of the week publication-title: Journal of the American College of Cardiology – volume: 18 start-page: 114 year: 2018 end-page: 123 article-title: A thiol‐reactive Ru (II) ion, not CO release, underlies the potent antimicrobial and cytotoxic properties of CO‐releasing molecule‐3 publication-title: Redox Biology – volume: 116 start-page: 1 year: 2021 end-page: 16 article-title: Omecamtiv mecarbil evokes diastolic dysfunction and leads to periodic electromechanical alternans publication-title: Basic Research in Cardiology – volume: 14 start-page: 3215 year: 2023 end-page: 3228 article-title: Reassessing CORM‐A1: Redox chemistry and idiosyncratic CO‐releasing characteristics of the widely used carbon monoxide donor publication-title: Chemical Science – volume: 214 year: 2023 article-title: Plight of CORMs: The unreliability of four commercially available CO‐releasing molecules, CORM‐2, CORM‐3, CORM‐A1, and CORM‐401, in studying CO biology publication-title: Biochemical Pharmacology – volume: 92 start-page: 2476 year: 2007 end-page: 2490 article-title: Stiffness and fraction of myosin motors responsible for active force in permeabilized muscle fibers from rabbit psoas publication-title: Biophysical Journal – volume: 12 start-page: 16904 year: 2022 article-title: Sarco/endoplasmic reticulum calcium ATPase activity is unchanged despite increased myofilament calcium sensitivity in Zucker type 2 diabetic fatty rat heart publication-title: Scientific Reports – volume: 158 start-page: 1821 year: 2001 end-page: 1831 article-title: Heat stress contributes to the enhancement of cardiac mitochondrial complex activity publication-title: The American Journal of Pathology – volume: 97 start-page: 1141 year: 1991 end-page: 1163 article-title: Alterations in Ca2+ sensitive tension due to partial extraction of C‐protein from rat skinned cardiac myocytes and rabbit skeletal muscle fibers publication-title: The Journal of General Physiology – volume: 389 start-page: 197 year: 2017 end-page: 210 article-title: Acute myocardial infarction publication-title: Lancet – volume: 91 start-page: 309 year: 2001 end-page: 315 article-title: Exercise training increases the Ca sensitivity of tension in rat cardiac myocytes publication-title: Journal of Applied Physiology – volume: 111 start-page: 1002 year: 2012 end-page: 1011 article-title: Nitroxyl‐mediated disulfide bond formation between cardiac myofilament cysteines enhances contractile function publication-title: Circulation Research – volume: 33 start-page: 5636 year: 1994 end-page: 5640 article-title: Soluble guanylate cyclase from bovine lung: Activation with nitric oxide and carbon monoxide and spectral characterization of the ferrous and ferric states publication-title: Biochemistry – volume: 260 start-page: 4151 year: 1985 end-page: 4155 article-title: Kinetics of carbon monoxide binding to monomeric hemoproteins. Role of the proximal histidine publication-title: The Journal of Biological Chemistry – volume: 10 year: 2015 article-title: Identification of the mitochondrial heme metabolism complex publication-title: PLoS ONE – volume: 149 start-page: 1104 year: 2006 end-page: 1112 article-title: Positive inotropic effects of carbon monoxide‐releasing molecules (CO‐RMs) in the isolated perfused rat heart publication-title: British Journal of Pharmacology – volume: 9 year: 2020 article-title: From synthesis to utilization: The ins and outs of mitochondrial heme publication-title: Cells – volume: 299 year: 2023 article-title: Phosphorylation‐dependent interactions of myosin‐binding protein C and troponin coordinate the myofilament response to protein kinase a publication-title: The Journal of Biological Chemistry – volume: 111 start-page: 31 year: 2012 end-page: 41 article-title: Cell damage following carbon monoxide releasing molecule exposure: Implications for therapeutic applications publication-title: Basic & Clinical Pharmacology & Toxicology – volume: 99 start-page: 2978 year: 2010 end-page: 2986 article-title: The role of thin filament cooperativity in cardiac length‐dependent calcium activation publication-title: Biophysical Journal – volume: 9 year: 2020 article-title: Vasopressors and inotropes in acute myocardial infarction related cardiogenic shock: A systematic review and meta‐analysis publication-title: Journal of Clinical Medicine – volume: 9 start-page: 397 year: 1994 end-page: 402 article-title: Clinical evidence for stunned myocardium after coronary artery bypass surgery publication-title: Journal of Cardiac Surgery – volume: 10 year: 2021 article-title: The interplay between S‐glutathionylation and phosphorylation of cardiac troponin I and myosin binding protein C in end‐stage human failing hearts publication-title: Antioxidants (Basel, Switzerland) – volume: 162 start-page: 566 year: 2011 end-page: 573 article-title: Levosimendan improves calcium sensitivity of diaphragm muscle fibres from a rat model of heart failure publication-title: British Journal of Pharmacology – volume: 8 start-page: 5454 year: 2017 end-page: 5459 article-title: Norborn‐2‐en‐7‐ones as physiologically‐triggered carbon monoxide‐releasing prodrugs publication-title: Chemical Science – volume: 17 start-page: 438 year: 2020 end-page: 448 article-title: Inotropic agents and vasopressors in the treatment of cardiogenic shock publication-title: Current Heart Failure Reports – volume: 14 year: 2021 article-title: Proteomic and functional studies reveal detyrosinated tubulin as treatment target in sarcomere mutation‐induced hypertrophic cardiomyopathy publication-title: Circulation. Heart Failure – volume: 9 start-page: 2127 year: 2020 end-page: 2135 article-title: Studies towards non‐toxic, water soluble, vasoactive norbornene organic carbon monoxide releasing molecules. publication-title: The Journal of Organic Chemistry – volume: 73 start-page: 3333 year: 1976 end-page: 3337 article-title: Nature of O and CO binding to metalloporphyrins and heme proteins publication-title: Proceedings of the National Academy of Sciences of the United States of America – volume: 1 start-page: 359 issue: 5 year: 2020 end-page: 367 article-title: Caffeine and dobutamine challenge induces bidirectional ventricular tachycardia in normal rats publication-title: Heart Rhythm O2 – volume: 15 year: 2022 article-title: Novel small‐molecule troponin activator increases cardiac contractile function without negative impact on energetics publication-title: Circulation. Heart Failure – volume: 172 start-page: 4506 year: 2015 end-page: 4518 article-title: The novel cardiac myosin activator omecamtiv mecarbil increases the calcium sensitivity of force production in isolated cardiomyocytes and skeletal muscle fibres of the rat publication-title: British Journal of Pharmacology – volume: 402 start-page: 675 year: 2021 end-page: 691 article-title: Revisiting the interaction of heme with hemopexin publication-title: Biological Chemistry – volume: 34 start-page: 1622 year: 2020 end-page: 1635 article-title: Management of challenging cardiopulmonary bypass separation publication-title: Journal of Cardiothoracic and Vascular Anesthesia – volume: 57 start-page: 37 year: 2003 end-page: 47 article-title: Increased Ca −sensitivity of the contractile apparatus in end‐stage human heart failure results from altered phosphorylation of contractile proteins publication-title: Cardiovascular Research – volume: 19 start-page: 1 year: 2005 end-page: 24 article-title: CORM‐A1: A new pharmacologically active carbon monoxide‐releasing molecule publication-title: The FASEB Journal – volume: 295 start-page: H1669 year: 2008 end-page: H1683 article-title: Increased intracellular Ca and SR Ca load contribute to arrhythmias after acidosis in rat heart. Role of Ca /calmodulin‐dependent protein kinase II publication-title: American Journal of Physiology. Heart and Circulatory Physiology – volume: 173 year: 2021 article-title: Application of carbon monoxide in kidney and heart transplantation: A novel pharmacological strategy for a broader use of suboptimal renal and cardiac grafts publication-title: Pharmacological Research – volume: 81 start-page: 616 year: 1994 end-page: 622 article-title: Pharmacokinetics of intravenous milrinone in patients undergoing cardiac surgery publication-title: Anesthesiology – volume: 39 start-page: 8782 year: 2000 end-page: 8790 article-title: Interaction of cardiac troponin C with Ca sensitizer EMD 57033 and cardiac troponin I inhibitory peptide publication-title: Biochemistry – volume: 292 start-page: R810 year: 2007 end-page: R818 article-title: Sex‐based differences in myocardial contractile reserve publication-title: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology – volume: 486 start-page: 67 year: 2004 end-page: 74 article-title: The effects of levosimendan and OR‐1896 on isolated hearts, myocyte‐sized preparations and phosphodiesterase enzymes of the Guinea pig publication-title: European Journal of Pharmacology – volume: 106 start-page: 2235 year: 2021 end-page: 2247 article-title: Increased myofilament calcium sensitivity is associated with decreased cardiac troponin I phosphorylation in the diabetic rat heart publication-title: Experimental Physiology – volume: 10 start-page: 10052 year: 2020 article-title: Age, sex and overall health, measured as frailty, modify myofilament proteins in hearts from naturally aging mice publication-title: Scientific Reports – volume: 6 start-page: 422 year: 2000 end-page: 428 article-title: Carbon monoxide has anti‐inflammatory effects involving the mitogen‐activated protein kinase pathway publication-title: Nature Medicine – volume: 108 start-page: 979 year: 2008 end-page: 987 article-title: Perioperative use of dobutamine in cardiac surgery and adverse cardiac outcome: Propensity‐adjusted analyses publication-title: Anesthesiology – volume: 10 start-page: 676 year: 2021 end-page: 686 article-title: Inotropic therapies in heart failure and cardiogenic shock: An educational review publication-title: European Heart Journal Acute Cardiovascular Care – volume: 306 start-page: 163 year: 1993 end-page: 168 article-title: Heme binding to calmodulin, troponin C, and parvalbumin, as a probe of calcium‐dependent conformational changes publication-title: Archives of Biochemistry and Biophysics – volume: 540 start-page: 457 year: 2002 end-page: 467 article-title: Role of cyclic GMP‐dependent protein kinase in the contractile response to exogenous nitric oxide in rat cardiac myocytes publication-title: The Journal of Physiology – volume: 27 start-page: 1859 year: 1995 end-page: 1866 article-title: Cardiac troponin C as a target protein for a novel calcium sensitizing drug, levosimendan publication-title: Journal of Molecular and Cellular Cardiology – volume: 77 start-page: 107 year: 1995 end-page: 113 article-title: Effects of levosimendan, a cardiotonic agent targeted to troponin C, on cardiac function and on phosphorylation and Ca sensitivity of cardiac myofibrils and sarcoplasmic reticulum in Guinea pig heart publication-title: Circulation Research – volume: 274 start-page: 18989 year: 1999 end-page: 18996 article-title: Mechanism of iron transport to the site of heme synthesis inside yeast mitochondria publication-title: The Journal of Biological Chemistry – volume: 171 start-page: 5169 year: 2014 end-page: 5181 article-title: Inhibition of phosphodiesterase‐3 by levosimendan is sufficient to account for its inotropic effect in failing human heart publication-title: British Journal of Pharmacology – volume: 78 start-page: 3120 year: 2000 end-page: 3137 article-title: Different myofilament nearest‐neighbor interactions have distinctive effects on contractile behavior publication-title: Biophysical Journal – volume: 132 start-page: 1350 year: 2022 end-page: 1360 article-title: Treadmill running increases the calcium sensitivity of myofilaments in diabetic rats publication-title: Journal of Applied Physiology – volume: 125 start-page: 1437 year: 1998 end-page: 1444 article-title: Carbon monoxide is a major contributor to the regulation of vascular tone in aortas expressing high levels of haeme oxygenase‐1 publication-title: British Journal of Pharmacology – volume: 24 start-page: 669 year: 1992 end-page: 681 article-title: Ultrastructural quantitation of mitochondria and myofilaments in cardiac muscle from 10 different animal species including man publication-title: Journal of Molecular and Cellular Cardiology – volume: 192 start-page: 1015 year: 2000 end-page: 1026 article-title: Carbon monoxide generated by heme oxygenase 1 suppresses endothelial cell apoptosis publication-title: The Journal of Experimental Medicine – volume: 467 start-page: 1303 year: 2015 end-page: 1317 article-title: Sexual dimorphic response to exercise in hypertrophic cardiomyopathy‐associated MYBPC3‐targeted knock‐in mice publication-title: Pflügers Archiv – volume: 89 start-page: 248 year: 2015 end-page: 262 article-title: Heme‐induced contractile dysfunction in human cardiomyocytes caused by oxidant damage to thick filament proteins publication-title: Free Radical Biology & Medicine – volume: 134 start-page: 98 issue: 1535 year: 2021 article-title: Can carbon monoxide protect hypertrophic hearts against ischaemia‐reperfusion injury? publication-title: New Zealand Medical Journal – volume: 245 start-page: 259 year: 1971 end-page: 262 article-title: The purification of cardiac myofibrils with triton X‐100 publication-title: Biochimica et Biophysica Acta‐Bioenergetics – volume: 280 start-page: 277 year: 1997 end-page: 283 article-title: Mechanisms of the contractile effects of levosimendan in the mammalian heart publication-title: The Journal of Pharmacology and Experimental Therapeutics |
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| Snippet | Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes such as... Abstract Patients undergoing cardiopulmonary bypass procedures require inotropic support to improve hemodynamic function and cardiac output. Current inotropes... |
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| SubjectTerms | Calcium (intracellular) calcium sensitivity Carbon monoxide Cardiac arrhythmia Cardiomyocytes Cytotoxicity Heart Heart rate Heme Hemopexin Laboratory animals myofilament Original Phosphatase Phosphorylation |
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| Title | The carbon monoxide prodrug oCOm‐21 increases Ca2+ sensitivity of the cardiac myofilament |
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