Continuous monitoring of heart rate, breathing episodes and blood pres
sure showed that the cardio-respiratory response of carp exposed to ni
trite (water concentration, 1 mmol l(-1)) changes with length of expos
ure. The animals developed a severe methaemoglobinaemia over the first
24 h of nitrite exposure. The minor changes in plasma HCO3- and lacta
te concentration, suggest that the observed hyperventilatory response
was sufficient to maintain aerobic metabolism throughout most of the b
ody during this time. During the second 24-h period, the rate of breat
hing increased further and short periods of bradycardia and hypotensio
n were seen. Over this latter period, the animals increased their use
of anaerobic metabolism as illustrated by the mean 48 h blood lactate
concentration of 4.8 mmol l(-1), a greater than 10-fold increase over
pre-exposure values. The increase in blood lactate was accompanied by
the predicted metabolic acidosis, however, an alkalosis of respiratory
origin and buffering combined to keep the plasma pH absolutely stable
throughout the study. This study shows that as the blood oxygen suppl
y is reduced through the development of methaemoglobinaemia, cardio-re
spiratory compensation by the carp is probably adequate to maintain ti
ssue oxygenation for short periods of nitrite exposure. However, as ni
trite exposure proceeds past 24 h, the animals progress into a positiv
e feedback cycle where the high cost of additional ventilation rapidly
accelerates their oxygen deficit which cannot be repaid, because <25%
of their haemoglobin is available for oxygen binding. Additionally, o
ur data demonstrate a circadian rhythm of physiological response to ni
trite and contradict the hypothesis that catecholamine release promote
s CO2 retention in water breathing animals. (C) 1997 The Fisheries Soc
iety of the British Isles