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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Fish physiology and biochemistry 16 (1997), S. 1-10 
    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.
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  • 2
    ISSN: 1432-136X
    Keywords: Key words Hypercapnia ; Acid-base balance ; Ion regulation ; Blood gases ; Copper
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In order to evaluate the impact of water-borne copper on acid-base regulation in fresh water rainbow trout, chronically cannulated fish were exposed to copper (0.6 mg 1−1), hypercapnia (water PCO2 of 6 mmHg) or a combination of copper and hypercapnia, while a fourth untreated group served as the control. Blood samples obtained at 0 h, 4 h and 24 h were analysed for acid-base status, ion concentrations and respiratory parameters. Tissue samples from caudal skeletal muscle, liver and gill filaments were examined for intracellular acid-base status, ion- and water contents, and copper concentration. Exposure to copper alone elicited a small extracellular metabolic alkalosis, no changes in arterial PO2, and a minor decrease in plasma ion concentrations. Hypercapnia alone increased arterial PCO2 from approximately 2 mmHg to 7.2 mmHg, but the extracellular respiratory acidosis present at 4 h was almost completely compensated at 24 h due to an increase in plasma bicarbonate concentration [HCO3 −] from 8.1 mM to 24.4 mM. Combined exposure to hypercapnia and copper resulted in a slightly larger acidosis at 4 h, and the fish failed to restore extracellular pH at 24 h, because plasma [HCO3 −] only increased to 16.3 mM. Fish exposed to hypercapnia and copper also showed a delayed recovery of intracellular pH in skeletal muscle, compared to fish exposure to hypercapnia only. Thus, copper exposure impaired both extracellular and intracellular acid-base regulation during hypercapnia. When seen in connection with only minor effects of copper on osmoregulatory and respiratory parameters, the reduced ability to regulate acid-base suggests that acid-base regulation may be one of the most copper-sensitive branchial functions.
    Type of Medium: Electronic Resource
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