AbstractsThe ability of carp to recover from nitrite-induced methaemoglobinaemia and disturbances in potassium balance and cell volume was studied in vivo and in vitro. Nitrite accumulated to a plasma concentration of 3 mM during 2 days of nitrite exposure was eliminated from the plasma within 2-3 days in clean water. The nitrite-induced methaemoglobinaemia disappeared after 3 days of recovery. During nitrite exposure, K + was lost from the red blood cells (RBCs) and from skeletal muscle tissue, which led to reduced cell volume and an extracellular hyperkalaemia. Extracellular [K +] rose less than predicted if lost K + had remained in the extracellular space, suggesting further transport of K + to the environment. The intracellular K + and water content were restored after few days of recovery in clean water, but this was paralleled by development of an extracellular hypokalaemia. This shows that intracellular K + balance was reestablished at the expense of the extracellular compartment, and supports that an overall K + deficit resulted from K + loss to the environment during nitrite exposure. Ventricle tissue differed from skeletal muscle and RBCs by not loosing K + and by having increased sodium and water contents during nitrite exposure. These changes were corrected by recovery in nitrite-free water. In vitro addition of nitrite to blood with low 02 saturation induced metHb formation and RBC K + efflux. Subsequent reduction of metHb to functional Hb was similar in blood with low and high 02 tension. A net re-uptake of K + was observed only in RBCs with low 02 saturation and when metHb reached low values.

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