ISSN:
1573-5168
Keywords:
nitrite
;
recovery from nitrite intoxication
;
potassium balance
;
hyperkalaemia
;
hypokalaemia
;
methaemoglobinaemia
;
intracellular potassium and water contents
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
Notes:
Abstracts The ability of carp to recover from nitrite-induced methaemoglobinaemia and disturbances in potassium balance and cell volume was studiedin vivo andin 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 O2 saturation induced metHb formation and RBC K+ efflux. Subsequent reduction of metHb to functional Hb was similar in blood with low and high O2 tension. A net re-uptake of K+ was observed only in RBCs with low O2 saturation and when metHb reached low values.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00004535
