Presentation description

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia, which currently affects 6 million people in the US, projected to double by 2030 according to the CDC. AF is characterized as an erratic quivering of the atrial chambers, affecting the heart's ability to effectively pump blood. Patients with AF have a 5-fold increased risk of stroke, a 3-fold increased risk of developing heart failure and a 2-fold increased risk of mortality. Adrenergic signaling in the atria is an important modulator of intracellular Ca2+ homeostasis, and its disruption has a profound impact on AF. Since our lab uses zebrafish as an animal model to study atrial fibrillation, our objective was to optimize a protocol for adrenergic stimulation in the explanted zebrafish heart. To accomplish this we measured heart rate and contractile activity in wild type zebrafish hearts before and after treatment with two adrenergic agonists: epinephrine and isoproterenol. These two drugs target different adrenergic receptors, while isoproterenol is a β-adrenergic agonist, epinephrine affect both, α- and β-adrenergic receptors. We found that exposure to 500μM epinephrine results in a significant increase in heart rate in the explanted hearts, while 500μM isoproterenol only resulted in a slight increase in HR. We are now in the process of increasing the concentration of isoproterenol. Having a protocol to induce stress by adrenergic stimulation in zebrafish heart would be extremely useful to advance the study of cardiac arrhythmias. Next steps include utilizing this protocols in our transgenic lines to see if the response to stress is different that observed in the WT fish.