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  1. 14 Journal of Physiology and Pharmacology

  2. 2 Bulletin of the Veterinary Institute in Puławy

  3. 2 Folia Morphologica

  4. 2 Journal of Physiology and Pharmacology. Supplement

  5. 1 Archivum Immunologiae et Therapiae Experimentalis

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Autorzy help

  1. 3 Hancox J. C.

  2. 3 Papp J. G.

  3. 3 Varro A.

  4. 3 Zhang H.

  5. 2 El Harchi A.

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  1. 1 2020

  2. 3 2019

  3. 1 2016

  4. 3 2015

  5. 2 2014

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1
Content available remote

The human ether-a-go-go-related gene (hERG) current inhibition selectively prolongs action potential of midmyocardial cells to augment transmural dispersion

100%
Yasuda C., Yasuda S., Yamashita H., Okada J., Hisada T., Sugiura S.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 4
2
Content available remote

Human ventilatory efficiency and respiratory sinus arrhythmia during head-up tilt

100%
Brown S. J., Bryant M., Mundel T., Stannard S. R.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 4
771-780
Cardiac vagal withdrawal when moving from supine to an upright posture may be independent of respiratory sinus arrhythmia. Further, ventilatory efficiency of an upright lung may improve with clustering of heart beats during inhalation. We studied healthy human subjects (n=8, 6 male) during supine rest (SUP) and 80° head-up tilt (HUT). ECG and expired breath were sampled continuously to determine heart rate, mean and end-tidal (ET) fractional content (F) of O2 and CO2, tidal volume (VT) and breathing frequency (Bf). HUT increased heart rate (47±3 vs. 59±9 beats min-1, p<0.01), decreased the high frequency component of heart rate variability (8.76± vs. 7.07±1.12, p<0.05), and increased the ratio of low to high frequency components in the heart rate (0.62±0.6 vs. 1.79±2.07, p<0.05). HUT did not change VT, Bf, or minute ventilation (V'E), but decreased FCO2 (4.90±0.48 vs. 4.56±0.42 %, p<0.05) and FETCO2 (6.64±0.24 vs. 6.30±0.27 %, p<0.01). HUT increased the CO2 ventilatory equivalent (24.88±2.50 vs. 26.74±2.61, p<0.01). Mean heart rate during inhalation increased with HUT (26±3 vs. 34±6 beats min-1), with no change during exhalation. Increased clustering of heart beats during inhalation independent of a decrease in HF cardiac variability may partly offset decreases in ventilatory efficiency of an upright lung.
3
Content available remote

Dual effect of ethanol on inward rectifier potassium current IK1 in rat ventricular myocytes

86%
Bebarova M., Matejovic P., Pasek M., Simurdova M., Simurda J.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 4
4
Content available remote

Comparative effects of the short QT N588K mutation at 37 degrees Celsius on hERG Kplus channel current during ventricular, purkinje fibre and atrial action potentials: an action potential clamp study

86%
McPate M. J., Zhang H., Adeniran I., Cordeiro J. M., Witchel H. J., Hancox J. C.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 1
23-41
The short QT syndrome (SQTS) is a cardiac repolarisation disorder characterised by abbreviated QT intervals on the electrocardiogram and by an increased risk of atrial and ventricular arrhythmias and sudden death. The SQT1 variant involves a gain-of-function mutation (N588K) that impairs inactivation of the hERG (human ether-a-go-go-related gene) potassium channel and, thereby, increases current mediated by the rapid delayed rectifier potassium current (IKr) in the heart. Here, the action potential voltage clamp (AP clamp) technique was applied to Chinese Hamster Ovary cells expressing wild-type or N588K-hERG at 37°C, to compare effects of the N588K mutation on hERG current (IhERG) during ventricular, atrial and Purkinje fibre APs. The N588K mutation altered the IhERG profile during each AP type; increased maximal repolarising current occurred earlier during AP repolarisation (with shifts of ~+60 mV, +30 mV and +15 mV respectively for ventricular, Purkinje fibre and atrial APs). Thus SQT1 may influence repolarising IhERG for each cell type, with AP clamp experiments and simulation data indicating the greatest effect during ventricular APs. Changes in the timing of outward IhERG transients elicited by premature stimuli following AP commands indicate that SQT1 may alter the protection that hERG provides cardiac tissue against premature arrhythmogenic stimuli.
5
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Application of ventricular tachyarrhythmia definitions of the updated Lambeth Conventions provides incompatibility with earlier results, masks antifibrillatory activity and reduces inter-observer agreement

86%
Regev A., Takacs H., Farkas A. S., Rarosi F., Polyak A., Papp H., Ivany E., Papp J. G., Varro A., Farkas A.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 1
6
Content available remote

Comparison of the efficiency of Na+/Ca2+ exchanger or Na+/H+ exchanger inhibition and their combination in reducing coronary reperfusion-induced arrhythmias

86%
Szepesi J., Acsai K., Sebok Z., Prorok J., Pollesello P., Levijoki J., Papp J. G., Varro A., Toth A.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 2
7

A microscopic view of false tendons in the left ventricle of the human heart

86%
Lotkowski D., Grzybiak M., Kozlowski D., Budzyn K., Kuta W.
Folia Morphologica
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1997
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tom 56
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nr 1
8

Morphology of the atrioventricular node in relation to the mechanism of atrioventricular nodal reentry tachycardia - a preliminary report

86%
Kozlowski D., Kozluk E., Kolodziej P., Grochowski P., Grzybiak M., Walczak F.
Folia Morphologica
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1996
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tom 55
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nr 4
9
Content available remote

Signal-averaged P-wave ECG as a marker of atrial electrical instability in patients with right ventricular dysfunction

72%
Schueller P. O., Steiner S., Enayat M., Schannwell C. M., Hennersdorf M., Strauer B. E.
Journal of Physiology and Pharmacology. Supplement
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2007
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tom 58
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nr 5
10
Content available remote

Hyperventilation assists proarrhythmia development during delayed repolarization in clofilium-treated, anaesthetized, mechanically ventilated rabbits

72%
Papp H., Sarusi A., Farkas A. S., Takacs H., Kui P., Vincze D., Ivany E., Varro A., Papp J. G., Forster T., Farkas A.
Journal of Physiology and Pharmacology
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2016
|
tom 67
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nr 5
11
Content available remote

Pathophysiological mechanism of cardiac arrhytmias as a key for optimal nonpharmacological treatment

72%
Kozluk E.
Journal of Physiology and Pharmacology. Supplement
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2006
|
tom 57
|
nr 11
69-77
Pathological automatism and triggered activity had focal origin. Thus, the treatment has to be aimed at ablation of the arrhythmogenic region. Some arrythmogenic places can be precisely characterized by analysis of ECG patterns. Among them are foci located close to the pulmonary veins, sinus node, ventricular outflow tracts or mitroaortic commissura. Classical ablation of these loci is highly successful. In other types of focal arrhythmias electroanatomical systems make possible to create 3D map, with activation sequence allowing for identification of the place where the arrhythmia could be eliminated. In reentrant mechanism of the arrhythmia the impulse circulates around the loop via the cardiac muscle. In case of the atrioventricular nodal reentrant tachycardia, atrial flutter or bundle branch ventricular tachycardia the loop can be easily outlined. Ablation can be performed using the anatomical method without induction of the tachycardia. In patients with the ventricular tachycardia with multiple forms or hemodynamically unstable it is possible to perform electranatomical map with visualization of the scar and the border zones. In this case the proarrhythmic region in the borderline zone is the aim of linear ablation without induction of tachycardias. In the chaotic tachycardias (atrial or ventricular fibrillation), the arrythmogenic substrate is too much dispersed to destroy them. Therefore, the ablation is aimed at the trigger which is initiating the arrhythmia (for instance the pathological Purkinje fibers). The excitability of the substrate may be also modified by pacemakers (ventricular or atrial resynchronization). In the life-threatening arrhythmias implantable cardioverter-defibrillator is necessary.
12
Content available remote

Serum fatty acid binding proteins as a potential biomarker in atrial fibrillation

72%
Golaszewska K., Harasim-Symbor E., Polak-Iwaniuk A., Chabowski A.
Journal of Physiology and Pharmacology
|
2019
|
tom 70
|
nr 1
13
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Content available

Cardiac channelopathies - A too frequently trivialized problem?

72%
Urbanczuk M., Jaroszynski A.
Journal of Pre-Clinical and Clinical Research
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2015
|
tom 09
|
nr 1
14
Content available remote

The s140g KCNQ1 atrial fibrillation mutation affects 'IKs' profile during both atrial and ventricular action potentials

72%
El Harchi A., Zhang H., Hancox J. C.
Journal of Physiology and Pharmacology
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2010
|
tom 61
|
nr 6
15
Content available remote

A new face of endocannabinoids in pharmacotherapy. Part I: Protective role of endocannabinoids in hypertension and myocardial infarction

72%
Zubrzycki M., Liebold A., Janecka A., Zubrzycka M.
Journal of Physiology and Pharmacology
|
2014
|
tom 65
|
nr 2
16

The role of polymorphonuclear neutrophils in myocardial damage during ischemia and reperfusion

72%
Wysocki H.
Archivum Immunologiae et Therapiae Experimentalis
|
1992
|
tom 40
|
nr 1
17

Paroxysmal atrial arrhythmias as a cause of syncope in a Boxer dog - a case report

72%
Noszczyk-Nowak A., Gajek J., Paslawska U., Rabczynski J., Slawuta A., Nicpon J.
Bulletin of the Veterinary Institute in Puławy
|
2008
|
tom 52
|
nr 1
The aim of the presented electrophysiological and histological study was the investigation of unexplained syncopal spells in a dog of Boxer breed. The dog underwent non-invasive procedures, which turned out to be insufficient for a complete diagnosis. Invasive procedures showed paroxysmal atrial fibrillation. In post-mortem examination, intensive extravascular fibrosis in the both atria, mostly in the endocardium, as well as a local loss of the cross-striation in cardiomyocytes, the presence of giant nuclei, and penetration of adipose tissue, especially in the left ventricle, were found. These changes might be the cause of arrhythmias. Paroxysmal atrial arrhythmias can be the mechanism of syncope in dogs. The electrophysiological properties of the myocardium predispose to both supraventricular and ventricular arrhythmias in dogs. Invasive electrophysiological study is a valuable diagnostic tool in dogs with syncope.
18

Clinical trials using autologous bone marrow and peripheral blood-derived progenitor cells in patients with acute myocardial infarction

72%
Tendera M., Wojakowski W.
Folia Histochemica et Cytobiologica
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2005
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tom 43
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nr 4
19

Arrhythmias in programmed electrical stimulation in the course of experimentally induced hyperthyroidism in an animal model

72%
Noszczyk-Nowak A., Gajek J., Paslawska U., Skrzypczak P., Zysko D., Nicpon J.
Bulletin of the Veterinary Institute in Puławy
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2008
|
tom 52
|
nr 1
To determine changes in physiological parameters of the myocardium in experimentally induced hyperthyreosis in an animal model, the occurrence and type of arrhythmias triggered during programmed electrical stimulation and changes in electrophysiological parameters of ventricular cardiomyocytes with hypertrophy due to hyperthyreosis were investigated. Hyperthyreosis was induced experimentally in five pigs, which were orally administered L-thyroxine at a dose of 20 µg/kg. Five untreated pigs served as the control. Programmed electrical stimulation was performed before administration of L-thyroxine (EPS 1), four (EPS 2) and eight (EPS 3) weeks after the onset of thyroxine administration, and four weeks after drug withdrawal (EPS 4). After the last stimulation, the animals were sacrificed and necropsied, with particular regard to heart autopsy. During the EPS 2, VERP was decreased in the group treated with the hormone (P<0.05). The mean values of AERP and AVNERP in the group were decreased as well. Atrial flutter and atrial fibrillation were induced during stimulation of the experimental group. In the other pigs of the experimental group, singular and paired ventricular extrasystolic were observed. In the EPS 3, AERP and AVNERP were statistically shorter in pigs with hyperthyreosis. A significant difference in Wenckebach CL between the control and experimental groups were observed. SNRT was shorter in the group with hyperthyreosis. In all pigs with hyperthyreosis, atrial fibrillation was induced. In one pig, non-sustained ventricular tachycardia was observed. During EPS 4, AERP remained shorter in group with hyperthyreosis. In two pigs of the group, atrial fibrillation was induced during pacing, and in two pigs, ventricular fibrillation was observed. The assessment of the heart's weight revealed a significant increase in its mass in pigs with hyperthyreosis. An increase in the thickness of the right and left ventricle free walls (P<0.01) and interventricular septum (P<0.01) was found in pigs with hyperthyreosis. At the same time, the inner diameter of the left ventricle was significantly smaller in this group (P<0.01) due to a concentric hypertrophy of the ventricle. In view of these findings, experimental hyperthyreosis caused shortening of refractory periods of different parts of the conducting system and enhanced susceptibility to supraventricular and ventricular arrhythmias, both spontaneous and induced during electrical stimulation. The mechanism of these arrhythmias can differ as a consequence of the hypertrophy of the left ventricle.
20

Cardiac ion channel gene mutations in Greek long QT syndrome patients

58%
Kotta C.-M., Anastasakis A., Gatzoulis K., Papagiannis J., Geleris P., Stefanadis C.
Journal of Applied Genetics
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2010
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tom 51
|
nr 4
The long QT syndrome (LQTS) is an inherited cardiac arrhythmia that may lead to sudden death in the absence of structural heart disease. Mutations in the cardiac potassium and sodium channel genes can be found in approximately 70% of patients with a highly probable clinical diagnosis. In this study, we aimed to genotype and explore the yield of genetic testing of LQTS patients from Greece, for whom there are no collective published data available. We clinically evaluated and genetically screened 17 unrelated patients for mutations in the KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 cardiac ion channel genes. Genetic testing was positive in 6 out of 8 patients with a highly probable clinical diagnosis of LQTS and negative for all the other patients. Two patients carried KCNQ1 mutations (c.580G>C, c.1022C>T), while 4 patients carried KCNH2 mutations (c.202T>C, c.1714G>A, c.3103delC, c.3136C>T). To the best of our knowledge, the last mentioned mutation (c.3136C>T) is novel. Moreover, 27 single-nucleotide polymorphisms (SNPs) were detected, 5 of which are novel. Our preliminary data indicate a low genetic diversity of the Greek LQTS genetic pool, and are in accordance with international data that genetic testing of the major LQTS genes is efficient in genotyping the majority of patients with a strong clinical diagnosis. Therefore, the transition of an LQTS genetic screening program from research to the diagnostic setting within our ethnic background is feasible.
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