Abstrakt

Relationship between electrophysiology and Ca2+ signalling in Goldfish intact hearts

Maedeh Bazmi, Ariel L Escobar

Fish have become an increasingly popular model to study cardiovascular physiology given its numerous advantages. However, many studies centred on the cardiac properties of Zebrafish (Denio rerio) are generally done in isolated cardiomyocytes and present limitations. This review evaluates the systolic Ca²⁺ signalling (Ca²⁺-T) parameters and the electrophysiological behaviour of intact Goldfish hearts, in order to establish a new fish model to study cardiovascular physiology. In this review we will discuss how Ca²⁺ signalling and the electrophysiological performance of Goldfish intact hearts were evaluated in comparison with Zebrafish using Local Field Fluorescence Microscopy (LFFM) and sharp microelectrode recordings. The hearts were perfused through the bulbus arteriosus with the Ca²⁺ indicator Rhod-2, among other solutions. Ventricular Action Potentials (APs) and Ca²⁺-T recorded from the Goldfish were considerably lengthier than those of the Zebrafish. Analysis of the Goldfish AP showed the half duration (APD50) of the ventricular AP heart was significantly longer (370.38 ± 8.8 ms) than the Zebrafish (83.9 ± 9.4 ms). Moreover, the half duration of the Ca²⁺-T was also much longer for Goldfish (266.9 ± 7.9 ms) than the Zebrafish (99.1 ± 2.7 ms). Blocking the L-type Ca²⁺ channel with Nifedipine in the Goldfish shortened both the APs and Ca²⁺-T. The AP Duration (APD) in the Goldfish hearts shortened with increasing temperature, and not surprisingly, Ryanodine and Thapsigargin perfusion significantly reduced the amplitude of epicardial Ca²⁺-T and prolonged the AP duration, indicating Ca²⁺ dependent inactivation of the L-type Ca²⁺ channels. These data suggest the electrophysiological properties and Ca²⁺-T in intact Goldfish hearts are more similar to those in the human heart endocardium, especially when compared with other fish models such as the Zebrafish. The central objective of this review is to discuss the strengths of the Goldfish as a new model to study cardiac signalling, and ultimately human cardiac pathology.