Oil exposure impairs in situ cardiac function in response to β-adrenergic stimulation in Cobia (Rachycentron canadum).

Aqueous crude oil spills expose fish to varying concentrations of dissolved polycyclic aromatic hydrocarbons (PAHs), which can have lethal and sublethal effects. The heart is particularly vulnerable in early life stages, as PAH toxicity causes developmental cardiac abnormalities and impaired cardiovascular function. However, cardiac responses of juvenile and adult fish to acute oil exposure remain poorly understood. We sought to assess cardiac function in a pelagic fish species, the cobia (Rachycentron canadum), following acute (24 h) exposure to two ecologically I relevant levels of dissolved PAHs. Cardiac power output (CPO) was used to quantify cardiovascular performance using an in situ heart preparation. Cardiovascular performance was varied using multiple concentrations of the beta-adrenoceptor agonist isoproterenol (ISO) and by varying afterload pressures. Oil exposure adversely affected CPO with control fish achieving maximum CPO's (4 mW g(-1) Mv) greater than that of oil-exposed fish (1 mW g(-1) Mv) at ISO concentrations of 1 x 10(-6) M. However, the highest concentration of ISO (1 x 10(-5) M) rescued cardiac function. This indicates an interactive effect between oil-exposure and beta-adrenergic stimulation and suggests if animals achieve very large increases in beta-adrenergic stimulation it could play a compensatory role that may mitigate some adverse effects of oil exposure in vivo.