Thesis supervisor: János Prorok
Web address (URL): http://web.med.u-szeged.hu/phcol/index.htm Location of studies (in Hungarian): Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Szeged Abbreviation of location of studies: ÁOK
Description of the research topic:
Triggered arrhythmias in cardiac muscle and intracellular Ca2+ have been linked since a long time. Today are known a number of trigger that show clear Ca2+ dependence but also there are a number of indicator whose mechanism appears to be linked to Ca2+-dependent processes. Fortunately, a number of different processes are needed at the same time to initiate of arrhythmogenesis in the human heart. For example hypokalemia (HK) may result from diuretic treatment, vomiting, diarrhea or strong exercise and is a common risk factor of ventricular arrhythmias and sudden cardiac death in elderly patients or in young athletes. HK decreases the Na+-K+-ATP-ase activity, leading to elevated intracellular Na+. This may elevate the cellular Ca2+ through activation of reverse mode Na+/Ca2+-exchanger (NCX), which may contribute to the increased arrhythmia risk. Furthermore, it is known, that strong physical exercise in competitive athletes induces adaptation of the cardiovascular system that involves lower resting heart rate, increased cardiac mass (hypertrophy) and volume, a phenomenon that is commonly referred to as „ the athlete’s heart”. Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in young competitive athletes according to autopsy findings. It has been known from previous studies that NCX activity is affected in various pathophysiological conditions of the heart. For this reason, we investigated the putative protective effect of selective NCX inhibition against arrhythmias caused by high intracellular Na+-induced Ca2+ overload, in various type of arrhythmia model.
Required language skills: English Further requirements: TDK munka