antiarrhythmic/hypoxie

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Class III antiarrhythmic action by potassium channel blockade: dofetilide attenuates hypoxia induced electromechanical changes.

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OBJECTIVE The aim was to examine the electromechanical effects of dofetilide, a new class III antiarrhythmic agent, in isolated guinea pig ventricular muscle during hypoxia. METHODS Hypoxia was induced by superfusing guinea pig right ventricular papillary, muscles with Tyrode's solution gassed with

Teratogenicity of the class III antiarrhythmic drug almokalant. Role of hypoxia and reactive oxygen species.

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The class III antiarrhythmic drug almokalant (ALM) was given to pregnant rats on Gestation Day 11 (125 micromol/kg) or 13 (25 micromol/kg). Other groups were pretreated with alpha-phenyl-N-t-butylnitrone, (PBN; 850 micromol/kg intraperitoneally) 1 h before administration of ALM or given

Cardiac antiarrhythmic evaluation of naloxone with or without propranolol using a modified chloroform-hypoxia screening test in the rat.

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The effects of naloxone and propranolol on cardiac arrhythmias and durations from respiratory arrest to ventricular asystole and cardiac standstill were studied in unanaesthetized young rats induced to suffer respiratory arrest and exhibit ventricular fibrillation (VF) by a modified chloroform

The anti-arrhythmic effect of chronic intermittent hypobaric hypoxia in rats with metabolic syndrome induced with fructose.

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This study investigated the anti-arrhythmic effects from chronic intermittent hypobaric hypoxia (CIHH) and the cellular mechanisms in rats with metabolic syndrome. Male Sprague-Dawley rats were randomly distributed among the control, fructose-fed (fed with 10% fructose in the drinking water to

Antiarrhythmic and electrophysiological actions of flecainide, bepridil and amiodarone on isolated heart preparations during controlled hypoxia.

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A model of arrhythmias based on the application of sinusoidal alternating current (ac) to isolated heart preparations has been employed to determine the effects of hypoxia (30 vol % O2 in the perfusion medium) on the threshold of arrhythmia and asystole. With this method three representatives of

Changes in phosphorylation of connexin43 in rats during acute myocardial hypoxia and effects of antiarrhythmic peptide on the phosphorylation.

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In order to confirm the hypothesis that during acute hypoxia, the antiarrhythmic peptide (AAP10) could improve conductance by changing the phosphorylation state of connexin43 (Cx43), isolated perfused rat hearts were randomly divided into three groups: control, hypoxia and AAP10 (n=9 in each group).

[Modulation of the antiarrhythmic effect by endogenous opioids during adaptation to hypoxia in rats].

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Adaptation of rats to hypoxia increased the heart resistance against arrhythmogenic effects. The Met-enkephaline-Arg6-Phe7 contant increased in the hypothalamus of the adapted animals. The blockers of mu- and delta-opioid receptors reduced the antiarrhythmic effect of the adaptation, whereas

[The role of changes in the bioelectrical activity of the cardiomyocytes in the antiarrhythmic effect of adaptation to hypobaric hypoxia].

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The adaptation to periodic hypoxia increases the AP duration in the cardiomyocytes of the rat isolated cardiac papillary muscles; prevents the depression of the resting potential, of the AP amplitude and duration in high calcium concentration and high-frequency stimulation. The adaptation also

Effects on rabbit nodal, atrial, ventricular and Purkinje cell potentials of a new antiarrhythmic drug, cibenzoline, which protects against action potential shortening in hypoxia.

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1 The effects of cibenzoline (UP 339-01), a new anti-arrhythmic drug, have been investigated in various cardiac tissues. 2 UP 339-01 produced a bradycardia, due partly to prolongation of the intracellularly recorded sinus node action potential duration (APD) and partly to depression of the maximum

[Significance of ATP-sensitive K(+)-channel in the mechanism of antiarrhythmic and cardioprotective effect of adaptation to intermittent hypobaric hypoxia].

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Adult male Wistar rats were exposed to intermittent hypobaric hypoxia (5000 m, 6 h/day, 6 weeks). It has been found that such mode of adaptation increased cardiac tolerance to arrhythmogenic action of a 45-min coronary artery occlusion but did not change an infarct size/area at risk (IS/AAR) ratio.

Role of ATP-sensitive K(+)-channels in antiarrhythmic and cardioprotective action of adaptation to intermittent hypobaric hypoxia.

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Mature Wistar rats were exposed to intermittent hypobaric hypoxia (5000 m, 6 h/day, 30 sessions). This mode of adaptation enhanced heart tolerance to the arrhythmogenic action of 45-min coronary occlusion, but does not affect the infarction size/risk area ratio. In some series, the rats were exposed

[Antiarrhythmic and antioxidative effects of intermittent hypoxia exposure on rat myocardium].

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The purpose of the study was to observe the effects of intermittent hypoxia exposure (IH) on the arrhythmia and antioxidation with ligation of coronary artery of rat heart together with measuring SOD (superoxide dismutase) and MDA (malondialdehyde) in myocardium. Comparison with continued hypoxia

The antiarrhythmic effect of adaptation to intermittent hypoxia.

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There was shown an antiarrhythmic effect of adaptation to intermittent hypobaric hypoxia in ischemia, reperfusion, experimental infarction and postinfarction cardiosclerosis (F.Z. Meerson, 1988). These results was obtained in whole animal experiments. In our study it was demonstrated that the

Preservation of TSPO by chronic intermittent hypobaric hypoxia confers antiarrhythmic activity.

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Abnormal activation of mitochondrial translocator protein (TSPO) contributes to arrhythmogenesis during cardiac metabolic compromise; however, its role in the antiarrhythmic activities of chronic hypoxia adaptation remains unclear. Our results demonstrated that 80% of normoxic rats developed

Involvement of Autonomic Nervous System in Antiarrhythmic Effect of Intermittent Hypobaric Hypoxia.

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We studied the involvement of the autonomic nervous system in the antiarrhythmic effect of intermittent hypobaric hypoxia modeled by daily placing the rats into an altitude chamber at 405 mm Hg (5000 m above sea level). The antiarrhythmic effect of hypoxia was observed on the model of acute coronary

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