Hypoxia and mercury contamination often co-occur in tropical freshwater ecosystems, but the interactive effects of these two stressors on fish populations are poorly known. The effects of mercury (Hg) on recorded changes in the detailed form of the electrocardiogram (ECG) during exposure to progressive hypoxia were investigated in two Neotropical freshwater fish species, matrinxã, Brycon amazonicus and traíra, Hoplias malabaricus. Matrinxã were exposed to a sublethal concentration of 0.1 mg L-1 of HgCl2 in water for 96 h. Traíra were exposed to dietary doses of Hg by being fed over a period of 30 days with juvenile matrinxãs previously exposed to HgCl2, resulting in a dose of 0.45 mg of total Hg per fish, each 96 h. Both species showed a bradycardia in progressive hypoxia. Hg exposure impaired cardiac electrical excitability, leading to first-degree atrioventricular block, plus profound extension of the ventricular action potential (AP) plateau. Moreover, there was the development of cardiac arrhythmias and anomalies such as occasional absence of QRS complexes, extra systoles, negative Q-, R- and S-waves (QRS complex), and T wave inversion, especially in hypoxia below O2 partial pressures (PO2) of 5.3 kPa. Sub-chronic dietary Hg exposure induced intense bradycardia in normoxia in traira, plus lengthening of ventricular AP duration coupled with prolonged QRS intervals. This indicates slower ventricular AP conduction during ventricular depolarization. Overall, the data indicate that both acute waterborne and sub-chronic dietary exposure (trophic level transfer), at sublethal concentrations of mercury, cause damage in electrical stability and rhythm of the heartbeat, leading to myocardial dysfunction, which is further intensified during hypoxia. These changes could lead to impaired cardiac output, with consequences for swimming ability, foraging capacity, and hence growth and/or reproductive performance.
Keywords: Cardiac electrical excitability; Electrocardiogram; Fish; Heavy metal; Low dissolved oxygen.