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  • 1
    ISSN: 1432-1793
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Cod (Gadus morhua) were exposed to hypercapnia (water Pco2 = 7.5 mmHg), elevated copper level (0.4 ppm) or a combination of both in order to study extra- and intracellular acid-base regulation and the influence hereupon of copper. During pure hypercapnia, the extracellular respiratory acidosis was completely compensated within 12 to 24 h via a chloride-mediated increase in extracellular [HCO3 −]. Exposure to copper in normocapnic seawater caused a large and progressive increase in plasma [Na+] and [Cl−] and a metabolic acidosis. Exposure to copper in hypercapnic seawater was associated with smaller elevations of plasma [Na+] and [Cl−] than in normocapnic seawater, showing that hypercapnia had a protective effect on the copper-induced osmoregulatory disturbances. The compensation of the hypercapnic acidosis was, however, slow and incomplete in fish exposed to both copper and hypercapnia. Extracellular pH remained depressed by 0.3 pH units after 72 h. The data reveal that acid-base regulation was immediately and persistently inhibited by copper. The limited acid-base regulation during combined copper and hypercapnia exposure was chloride-mediated as during hypercapnia alone. Intracellular pH recovery was complete and very rapid in ventricular and skeletal muscle tissues during environmental hypercapnia, whereas acid-base compensation in liver tissue was slower, the kinetics being similar to that in the extracellular compartment. Intracellular pH compensation was significantly slowed down by copper. Copper concentration increased drastically in gill tissue already at 3 h, while copper concentrations in liver, muscle and plasma were significantly elevated only after 48 h, with liver showing the largest elevation.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of fish biology 42 (1993), S. 0 
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Transfer of rainbow trout from fresh water to 20‰ sea water decreased dorsal aortic Po2 from 90 to 60 mmHg within 1 h. Arterial Po2 was depressed for 24 h before it returned to control values. The internal hypoxia rapidly reduced the red cell nucleoside triphosphate content, suggesting prompt regulation of blood O2 affinity. The extracellular acid-base status changed towards a small mixed metabolic and respiratory acidosis.
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  • 3
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 50 (1988), S. 161-179 
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of fish biology 40 (1992), S. 0 
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Endogenous levels of TXB2 and 6-keto PGF1a are reported in dorsal aortic blood from rainbow trout. Acute hypoxia induced an increase in TXB2 levels whereas 6-keto PGF1a was unaffected. We suggest that enhanced thromboxane synthesis might have a role in microcirculation of various organs in fish hypoxia.
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of fish biology 62 (2003), S. 0 
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Carbon dioxide transport in African lungfish Protopterus aethiopicus blood conformed to the typical vertebrate scheme, implying a crucial and rate-limiting role of erythrocyte Cl–/HCO3– exchange. The rate coefficient for unidirectional Cl– efflux via the anion exchanger (k, s−1) increased with temperature in African lungfish, but values were well below those reported in other species. The erythrocytes of African lungfish were, however, very large (mean cellular volume = 6940 µm3), and the ratio of cell water volume to membrane surface area was high (VwAm−1 = 1·89). Hence, the apparent Cl– permeability (PCl = kVwAm−1, µm s−1) was close to that in other vertebrates. The plot of lnPCl against the inverse absolute temperature was left-shifted in the tropical African lungfish compared to the temperate rainbow trout Oncorhynchus mykiss, which supports the idea that PCl is similar among animals when compared at their preferred temperatures. Also, Q10 for anion exchange calculated from PCl values in African lungfish was 2·0, supporting the idea that the temperature sensitivity of erythrocyte anion exchange matches the temperature sensitivity of CO2 production and transport in ectothermic vertebrates.
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of fish biology 59 (2001), S. 0 
    ISSN: 1095-8649
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: 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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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Fish physiology and biochemistry 16 (1997), S. 157-170 
    ISSN: 1573-5168
    Keywords: acid-base regulation ; pH compensation ; hypercapnia ; calcium ; bicarbonate ; chloride ; ventilation ; bicarbonate accumulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The influence of ambient calcium, bicarbonate and chloride levels on acid-base regulation was investigated in rainbow trout acclimated and exposed to hypercapnia in five different water types. In soft water (low [Ca++] and [HCO3 −]), compensation of the respiratory acidosis was slow and incomplete within 72h. High ambient [HCO3 −] clearly improved extracellular HCO3 − accumulation, and pH recovery was accomplished within 24h. This may result from stimulation of branchial HCO3 − (influx)/Cl− (outflux) exchange. Elevation of ambient [Cl−] had a small, positive effect on pH compensation. High ambient [Ca++] improved the degree of pH compensation. Plasma [HCO3 −] and [Cl−] showed an inverse 1:1 relationship in all acclimation groups, revealing an ubiquitous chloride-mediated acid-base regulation. Ventilation activity was increased by hypercapnia and only returned to control values in hard water (high [HCO3 −]and [Ca++]). During progressive hypercapnia (up to 3% CO2), hard water acclimated fish obtained significantly higher plasma [HC03 −] (51.2 mM) than fish acclimated to low [Ca++]/high [HCO3 −] (44.7 mM). This suggests an additive effect of ambient Ca++ on plasma HCO3 − accumulation. At levels of CO2 above 1%, some mortality was induced in low [Ca++]/high [HCO3 −] water. Dying fish could be distinguished from surviving fish by an excessive Cl−loss and increasing extracellular anion gap.
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  • 8
    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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  • 9
    ISSN: 1432-136X
    Keywords: Gill Na+, K+-ATPase ; Oxygen uptake ; Plasma and red blood cell pH ; Fresh water to seawater transfer ; Whitefish, Coregonus lavaretus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Osmoregulation, acid-base balance and respiratory parameters were investigated in whitefish following transfer from freshwater to salt water. Whitefish acclimated successfully to 25 ppt brackish water but died after direct transfer to 32 ppt sea water. Transfer to brackish water induced rapid (〈6 h) and permanent increases in plasma [Na+], [Cl−], total [Ca] and [Mg]. The extracellular hyperosmolality effected a transient (〈3 days) muscle tissue dehydration and red blood cell shrinkage. Exposure to brackish water decreased both the arterial O2 tension and whole body O2 uptake. The extracellular acid-base status changed from an initial respiratory acidosis at 1 h towards a pronounced metabolic acidosis at 48 h of brackish water exposure. Red cell pHi decreased in parallel with extracellular pHe, but the in vivo ΔpHi/ΔpHe was only 0.26, suggesting some selective protection of red cell pHi. Plasma cortisol concentration and gill Na+, K+-ATPase activity increased after exposure to high ambient salinity, reflecting the induction of hypo-osmoregulatory mechanisms. The physiological changes in whitefish are discussed in relation to salinity-induced effects in other salmonid fishes.
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  • 10
    ISSN: 1432-136X
    Keywords: Key words Acid-base regulation ; Anion uptake ; Nitrite ; DIDS ; bumetanide ; AbbreviationsDIDS 4,4′-diisothiocyanatostilbene-2,2′-disulfonate ; Jin influx ; Vmax maximal flux rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Nitrite influx into crayfish showed saturation kinetics, supporting a carrier-mediated uptake. Addition of 4,4′-diisothiocyanatostilbene-2,2′-disulfonate (DIDS: at 10−5, 10−4 and 10−3 M) and bumetanide (at 10−5 M and 10−4 M) to the ambient water did not significantly affect nitrite influx. Rather than suggesting that neither Cl−/HCO3 − exchange nor K+/Na+/2Cl− cotransport were involved in the transport, this may reflect that the gill cuticle has a low permeability to the pharmacological agents, or that the sensitivity of the transport mechanism to the inhibitors is low. Nitrite accumulation in the haemolymph was significantly decreased during hypercapnic conditions compared to normocapnic conditions. This supports the idea that an acid–base regulatory decrease in Cl−(influx)/HCO3 − (efflux) induced by hypercapnia should decrease NO2 − uptake if NO2 − and Cl− share this uptake route. The respiratory acidosis caused by exposure to hypercapnia alone was partially compensated by HCO3 − accumulation in the haemolymph. Combined exposure to hypercapnia and nitrite improved pH recovery, mainly by augmenting the [HCO3 −] increase, but also by decreasing haemolymph PCO2. Exposure to nitrite in normocapnic water induced an initial increase in haemolymph [HCO3 −] and later also a decrease in PCO2. Thus, the improved acid-base compensation during combined hypercapnia and nitrite exposure was an amplification of this nitriteinduced response. Haemolymph base excess rose much more than haemolymph [Ca], suggesting that transfer of acid-base equivalents between animal and water was more important than H+ buffering by exoskeletal CaCO3 in mediating the increase in haemolymph [HCO3 −].
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