Nitrite‐exposed (1 mM) rainbow trout Oncorhynchus mykiss fell into two distinct groups with regard to susceptibility and physiological response. Group 1 accumulated nitrite in plasma to a concentration of 2·9 mM within 24 h and died before 48 h. Group 2 survived for 96–144 h, and the accumulation of nitrite was slower, levelling off at a concentration c. 2·3 mM at 72 h. Methaemoglobin (metHb) formation was faster in group 1 than in group 2, but both groups had a metHb fraction c. 70% before dying. The extracellular electrolyte balance was perturbed significantly only in group 1, where plasma [Cl ‐ ] decreased and plasma [K + ] increased. Heart rate increased rapidly, more in group 1 than in group 2. The tachycardia occurred before any significant changes in metHb or [K + ] had developed, suggesting that it was due to nitrite‐induced vasodilation, possibly via nitric oxide generated from nitrite, that was countered by an increased cardiac pumping to re‐establish blood pressure. Arterial blood pressure and pulse pressure were accordingly kept reasonably constant. Heart rate variability was significantly depressed in group 1. The ventilation rate was significantly increased after 9 h of nitrite exposure in group 1, while the ventilation in group 2 did not increase significantly before 21 h. The data reveal that nitrite has substantial influence on the cardio‐respiratory function in fishes.
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Aggergaard et al. (2001) studied this question.
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