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antiarrhythmic/càries dental
L'enllaç es desa al porta-retalls
Pàgina 1 des de 52 resultats
[Rectal tenesmus due to tumor invasion into the pelvic cavity responding favorably to antiarrhythmic drug therapy].
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We experienced 3 patients(Cases 1, 3, and 4)with pelvic tumor-related rectal tenesmus showing favorable responses to antiarrhythmic drugs. Based on this experience, we administered antiarrhythmic drugs preferentially to 2 others with tumor derived rectal tenesmus(Cases 2 and 5), and again obtained
[Response to arrhythmic and antiarrhythmic agents of the automatic centers of different cardiac cavities].
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Identification of the A293 (AVE1231) Binding Site in the Cardiac Two-Pore-Domain Potassium Channel TASK-1: a Common Low Affinity Antiarrhythmic Drug Binding Site.
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Mutational analysis of block and facilitation of HERG current by a class III anti-arrhythmic agent, nifekalant.
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Chemicals and toxins are useful tools to elucidate the structure-function relationship of various proteins including ion channels. The HERG channel is blocked by many compounds and this may cause life-threatening cardiac arrhythmia. Besides block, some chemicals such as the class III anti-arrhythmic
Computer Simulations Reveal a Novel Blocking Mode of the hERG Ion Channel by the Antiarrhythmic Agent Clofilium.
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The binding modes of many hERG ion channel blockers are well understood, but a notable exception is clofilium, a potent antiarrhythmic agent whose action relies on blocking the current mediated by hERG. From the previously hypothesized binding modes of clofilium to hERG, only two can explain most of
Molecular determinants for high-affinity block of human EAG potassium channels by antiarrhythmic agents.
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Undesired block of human ERG1 potassium channels is the basis for cardiac side effects of many different types of drugs. Therefore, it is important to know exactly why some drugs particularly bind to these channels with high affinity. Upon expression in mammalian cells and Xenopus laevis oocytes, we
Molecular basis of hERG potassium channel blockade by the class Ic antiarrhythmic flecainide.
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The class Ic antiarrhythmic drug flecainide inhibits KCNH2-encoded "hERG" potassium channels at clinically relevant concentrations. The aim of this study was to elucidate the underlying molecular basis of this action. Patch clamp recordings of hERG current (IhERG) were made from hERG expressing
Antiarrhythmic Properties of Ranolazine: Inhibition of Atrial Fibrillation Associated TASK-1 Potassium Channels.
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Background: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and one of the major causes of cardiovascular morbidity and mortality. Despite good progress within the past years, safe and effective treatment of AF remains an unmet clinical need. The anti-anginal agent
High affinity HERG K(+) channel blockade by the antiarrhythmic agent dronedarone: resistance to mutations of the S6 residues Y652 and F656.
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Pharmacological inhibition of human-ether-a-go-go-related gene (HERG) K(+) channels by structurally and therapeutically diverse drugs is associated with the 'acquired' form of long QT syndrome and with potentially lethal cardiac arrhythmias. Two aromatic amino-acid residues (Y652 and F656) on the
Overlapping binding sites of structurally different antiarrhythmics flecainide and propafenone in the subunit interface of potassium channel Kv2.1.
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Kv2.1 channels, which are expressed in brain, heart, pancreas, and other organs and tissues, are important targets for drug design. Flecainide and propafenone are known to block Kv2.1 channels more potently than other Kv channels. Here, we sought to explore structural determinants of this
Pharmacophore and pseudoreceptor modelling of class Ib antiarrhythmic and local anaesthetic lidocaine analogues.
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A molecular modelling study was carried out in order to investigate the molecular binding behaviour of antiarrhythmically and local anaesthetically active aminoacylanilide derivatives from the lidocaine type at their specific sodium channel binding site. An examination of relevant X-ray structures
Kv1.5 open channel block by the antiarrhythmic drug disopyramide: molecular determinants of block.
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Kv1.5 is considered to be a potential molecular target for treatment of atrial fibrillation or flutter. Disopyramide is widely used in the treatment of atrial flutter and/or atrial fibrillation. The present study was undertaken to characterize the effects of disopyramide on currents mediated by
Inhibition of Voltage-Gated K+ Channel Kv1.5 by Antiarrhythmic Drugs.
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Molecular dynamics simulations are employed to determine the inhibitory mechanisms of three drugs, 5-(4-phenoxybutoxy)psoralen (PAP-1), vernakalant, and flecainide, on the voltage-gated K+ channel Kv1.5, a target for the treatment of cardiac arrhythmia. At neutral pH, PAP-1 is neutral, whereas the
Canine model of ventricular fibrillation using programmed stimuli and localized myocardial warming or cooling.
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The purpose of this study was to establish an animal model in which ventricular fibrillation (VF) can be induced reproducibly and defibrillation can be accomplished repeatedly. The left anterior descending artery (LAD) was cannulated and perfused with blood from the carotid artery in eleven
Pericardial prostaglandin biosynthesis prevents the increased incidence of reperfusion-induced ventricular fibrillation produced by efferent sympathetic stimulation in dogs.
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This study tested the hypothesis that sympathetic neural stimulation increases the prevalence of reperfusion-induced ventricular fibrillation and explored the mechanisms by which this occurs and how it may be prevented. In anesthetized, autonomically denervated dogs, we examined the effects of
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