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SzSA YearBook 2016/17

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SZENT-GYÖRGYI MENTORS<br />

ÁGNES VÉGH<br />

Haemodynamic Laboratory,<br />

Department of Pharmacology and Pharmacotherapy,<br />

Faculty of Medicine,<br />

University of Szeged<br />

Address: Dóm tér 12., H-6720 Szeged, Hungary<br />

E: vegh.agnes@med.u-szeged.hu<br />

T: +36 62/545-673<br />

RESEARCH AREA<br />

The problem of sudden cardiac death resulting from ventricular<br />

fibrillation during acute myocardial ischaemia is still<br />

the biggest challenge facing modern cardiology. As drug<br />

therapy has proved to be largely ineffective, understanding<br />

the underlying mechanisms that lead to these life-threatening<br />

ventricular arrhythmias is crucial for developing novel<br />

therapeutic strategies.<br />

Over the last 30 years our research has focused on to explore<br />

possibilities which are able to protect the heart against<br />

these severe often fatal arrhythmias. One of such possibilities<br />

is the phenomenon of preconditioning through<br />

which the heart is able to increase its tolerance against the<br />

consequences of a harmful, by itself fatal ischaemic stress.<br />

Efforts are made on to explore the triggers, the signalling<br />

pathways and end-effectors, which are likely to be involved<br />

in the preconditioning-induced cardioprotection. We attempt<br />

to establish protocols which might be useful in the<br />

therapy for the attenuation of the risk of sudden cardiac<br />

death.<br />

We address various questions using pharmacological<br />

approaches in in vivo animal studies and also in in vitro<br />

examinations by applying various biochemical and molecular<br />

biological methods. Such a comprehensive approach<br />

makes possible to assess processes which act and influence<br />

arrhythmogenesis in the whole body and count for these at<br />

cellular level.<br />

TECHNIQUES AVAILABLE IN THE LAB<br />

In vivo methods: Experiments in large animals – surgical<br />

interventions, measurements of basic haemodynamic,<br />

electrophysiological, blood flow and contractile function<br />

parameters.<br />

In vitro methods: immuno-blotting (e.g. Western blot), RT-<br />

PCR, image analysis (e.g. immunofluorescence confocal<br />

microscopy), immunoprecipitation, ELISA. Through our<br />

collaboration several other methods are available, e.g. SNO-<br />

RAC analysis, RIA.<br />

SELECTED PUBLICATIONS<br />

Gönczi, M., Kovács, M., Seprényi, Gy., Végh, Á. (2012) The<br />

involvement of gap junctions in the delayed phase of the<br />

ptotection induced by cardiac pacing in dogs. Clin Sci 123:<br />

39-51.<br />

Papp, R., Gönczi, M., Kovács, M., Seprényi, Gy., Végh, Á.<br />

(2007) Gap junctional uncoupling plays a trigger role in the<br />

antiarrhythmic effect of ischaemic preconditioning. Cardiovasc<br />

Res 74: 396-405.<br />

Babai, L., Szigeti, Zs., Parratt, J.R., Végh, Á. (2002) Delayed<br />

cardioprotective effects of exercise in dogs are aminoguanidine<br />

sensitive: possible involvement of nitric oxide.<br />

Clin Sci 102: 435-445.<br />

Végh, Á., Szekeres, L., Parratt, J.R. (1992) Preconditioning of<br />

the ischaemic myocardium; involvement of the L-arginine -<br />

nitric oxide pathway. Br J Pharmacology 107: 648-652.<br />

Végh, Á., Komori, S., Szekeres, L., Parratt, J.R. (1992) Antiarrhythmic<br />

effects of preconditioning in anaesthetized<br />

dogs and rats. Cardiovasc Res 26: 487-495.<br />

74

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