Calcium Sensitizer EMD 57033, But Not the β 1 -Adrenoreceptor Agonist Dobutamine, Increases Mechanical Efficiency in Stunned Myocardium

Trines, Serge A.; Smits, Carlo A. G.; Moer, Joost Van der; Slager, Cornelis J.; Verdouw, Pieter D.; Krams, Rob

doi:10.1097/00005344-200201000-00008

Cited by 5 publications

(2 citation statements)

References 18 publications

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“…In contrast, the inotropic effect of catecholamines is achieved by raising cytosolic Ca 2+ , which increases oxygen consumption. Mechanical efficiency (ratio of cardiac work/myocardial oxygen consumption) was significantly higher for the calcium sensitizer EMD 57033 than dobutamine in porcine stunned myocardium [33]. A decrease in contraction economy has also been shown with other catecholamines [34].…”

Section: Myocardioprotective Effect Of Levosimendanmentioning

confidence: 90%

Effects of Levosimendan on Myocardial Infarct Size and Hemodynamics in a Closed-Chest Porcine Ischemia–Reperfusion Model

Busk

Mæng

Kristensen

et al. 2006

Cardiovasc Drugs Ther

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Section: Myocardioprotective Effect Of Levosimendanmentioning

confidence: 90%

Effects of Levosimendan on Myocardial Infarct Size and Hemodynamics in a Closed-Chest Porcine Ischemia–Reperfusion Model

Busk

Mæng

Kristensen

et al. 2006

Cardiovasc Drugs Ther

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“…Studies in conscious dogs with and without induced heart failure showed a dramatic effect of EMD 57033 on contractility in both control and failed hearts with improvement of mechanical efficiency and without compromise of diastolic function [74]. Furthermore, studies with open chest pig hearts stressed by a stunning protocol, also demonstrated an improvement of contractility with improved mechanical efficiency [79]. A related study has shown that EMD 57033 is potently effective in acutely restoring systolic function in a mouse model harboring a proteolytic truncation of cTnI, cTnI , associated with myocardial stunning [80].…”

Section: Emd 57033mentioning

confidence: 95%

Interaction of cardiac troponin with cardiotonic drugs: A structural perspective

Robertson

Sykes

2008

Biochemical and Biophysical Research Communications

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Over the forty years since its discovery, many studies have focused on understanding the role of troponin as a myofilament based molecular switch in regulating the Ca 2+ -dependent activation of striated muscle contraction. Recently, studies have explored the role of cardiac troponin as a target for cardiotonic agents. These drugs are clinically useful for treating heart failure, a condition in which the heart is no longer able to pump enough blood to other organs. These agents act via a mechanism that modulates the Ca 2+ -sensitivity of troponin; such a mode of action is therapeutically desirable because intracellular Ca 2+ concentration is not perturbed, preserving the regulation of other Ca 2+ -based signaling pathways. This review describes molecular details of the interaction of cardiac troponin with a variety of cardiotonic drugs. We present recent structural work that has identified the docking sites of several cardiotonic drugs in the troponin C -troponin I interface and discuss their relevance in the design of troponin based drugs for the treatment of heart disease.

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Facile Synthesis of Carboxamide-Substituted 1,3,4-Thiadiazines and 5,6-Dihydro-4H-1,3,4-Thiadiazin-5-Ols

Komendantova

Ivanova

Lyssenko

et al. 2019

Chem Heterocycl Comp

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Calcium Sensitizer EMD 57033, But Not the β 1 -Adrenoreceptor Agonist Dobutamine, Increases Mechanical Efficiency in Stunned Myocardium

Cited by 5 publications

References 18 publications

Effects of Levosimendan on Myocardial Infarct Size and Hemodynamics in a Closed-Chest Porcine Ischemia–Reperfusion Model

Effects of Levosimendan on Myocardial Infarct Size and Hemodynamics in a Closed-Chest Porcine Ischemia–Reperfusion Model

Interaction of cardiac troponin with cardiotonic drugs: A structural perspective

Facile Synthesis of Carboxamide-Substituted 1,3,4-Thiadiazines and 5,6-Dihydro-4H-1,3,4-Thiadiazin-5-Ols

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