Abstract
The effects of microcystin on the cardio-respiratory function of Nile tilapia were analyzed 48h after intraperitoneal injection of microcystin-LR (MC-LR – 100μgkg−1body weight). Exposure to MC-LR induced significant reduction in metabolic rate (V˙O2) and increase in the critical O2 tension (PCO2) in relation to the control group. Gill ventilation (V˙G) and ventilatory tidal volume (VT) were considerably lower in fish exposed to MC-LR, probably due to an alteration in the homeostatic mechanisms, impairing the regular respiratory response of this species to environmental hypoxia. The ability to maintain the O2 extraction from the ventilatory current (EO2) during severe hypoxia was also significantly reduced in fish exposed to MC-LR exposure. Control fish displayed the characteristic reflex bradycardia in response to hypoxia. However, when compared to the control group, fish exposed to MC-LR presented significantly lower heart rate (fH) in normoxia and in all experimental hypoxic levels, probably due to a direct effect of this toxin on the cardiac tissue.
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