scholarly journals Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion

1986 ◽  
Vol 126 (1) ◽  
pp. 41-61 ◽  
Author(s):  
J. B. Claiborne ◽  
N. Heisler

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)

1983 ◽  
Vol 55 (4) ◽  
pp. 1187-1195 ◽  
Author(s):  
N. E. Madias ◽  
H. J. Adrogue

Previous studies from this laboratory have characterized the “whole-body” response to acute hypercapnia in normal dog and humans. A more recent investigation has demonstrated that this response is markedly altered by graded degrees of chronic respiratory acidosis. The present studies were carried out to assess the influence, if any, of chronic metabolic acid-base disturbances on the acute CO2 titration curve in the dog. To this purpose we first produced a broad range of chronic plasma bicarbonate concentration of metabolic nature. Metabolic acidosis (n = 14) was produced by prolonged HCl-feeding and metabolic alkalosis (n = 11) by diuretics and a chloride-free diet. Animals with normal acid-base status (n = 4) were also studied. After the establishment of a chronic steady state of acid-base equilibrium, we then performed an acute CO2 titration of the unanesthetized dogs within a large environmental chamber. Three levels of inspired CO2 fraction (FICO2) were employed ranging from 4 to 15%. The results indicate that chronic metabolic acid-base disturbances exert a dramatic influence on the whole-body response to acute hypercapnia. The acute change in plasma bicarbonate for a given change in partial pressure of CO2 in arterial blood (PaCO2) or plasma pH decreases as a function of the chronic level of plasma bicarbonate concentration. Yet the ability of the organism to defend plasma hydrogen ion concentration is progressively strengthened as the chronic level of plasma bicarbonate increases.(ABSTRACT TRUNCATED AT 250 WORDS)


1984 ◽  
Vol 108 (1) ◽  
pp. 25-43 ◽  
Author(s):  
J. B. CLAIBORNE ◽  
NORBERT HEISLER

Acid-base balance and ion transfers were studied in the carp, Cyprinus carpio L., during and after 48 h of exposure to environmental hypercapnia (PCOCO27.5 Torr). Plasma pH, PCOCO2, [HCO3−], and net transfers of HCO3−, NH4+, Cl− and Na+ between the fish and the environmental water were measured periodically throughout the experiment. Over the first 8 h of hypercapnia, plasma PCOCO2 increased by 7.6 Torr with a concurrent decrease in plasma pH of 0.28 units. Plasma [HCO3−] was slowly elevated from about 14 to 22 mM after 48 h, at which point 50% of the pH depression expected at constant bicarbonate concentration had been compensated. The net amount of H+ transferred to the water was 3.3 mmol kg−1 fish, representing a 115% increase in the rate of cumulative H+ efflux, and inducing an elevation of both intracellular and extracellular [HCO3−]. Cl− transfer was reversed from a net uptake to a net efflux, while net Na+ influx was increased slightly. Following hypercapnia, plasma pH returned to control values within 1 h, while the plasma [HCO3−], which was elevated during hypercapnia, fell continuously to reattain pre-hypercapnic control values after 20 h. The [HCO3−] decrease was due to the net gain of H+ ions from the water during this period. Cl− transfer returned to a net uptake, while the original Na+ influx was reversed to a net loss. Acid-base regulatory responses in the carp are qualitatively similar to those observed in other fish, though the time required for compensatory pH adjustment is longer. It is concluded that alterations in the rates of Cl−/HCO3− and Na+/H+ exchanges during hypercapnia and Na+/H+ exchange following hypercapnia, play a significant role in the compensation of respiratory acid-base disturbances in these animals.


1979 ◽  
Vol 82 (1) ◽  
pp. 331-344 ◽  
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS

An abrupt increase in ambient CO2, resulted in a marked respiratory acidosis which took place within 30 min. During this time there was a considerable reduction in the PCO2. difference between arterial blood and inspired gas caused by an increase in ventilations. Prolonged CO2 exposure (24 h) showed that there was some compensation for the acidosis in that plasma bicarbonate concentrations increased substantially. At the same time, however, the PCO2 of arterial blood always rose so that the net result was usually only a small increase in pH. Upon return to air, the blood was backtitrated along a buffer line elevated above and parallel to that seen during the initial response to hypercapnia. The fall in arterial blood PCO2, during the early stages of recovery often led to pH values higher than those seen in the untreated animal. After 48 h in air, recovery had gone further with PCO2 pH and [HCO3-] levels approaching but rarely reaching the pre-exposure values.


1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.


1981 ◽  
Vol 93 (1) ◽  
pp. 65-80
Author(s):  
G. R. Ultsch ◽  
M. E. Ott ◽  
N. Heisler

Carp (Cyprinus carpio) were exposed to environmental water pH (pHw) step changes from 7.4 to 5.1, 5.1 to 4.0 and 4.0 to 3.5 pH, PCO2, PO2 and lactate in dorsal aortic blood, [Na+], [K+] and [Cl-] in dorsal aortic plasma, base loss, and ammonia excretion were determined as a function of time after each pHw step change. At pHw 5.1 the measured blood acid-base and electrolyte parameters remained essentially unchanged; the base loss, however, was increased by a factor of 2. When pHw was lowered to 4.0 an additional severe increase in the ‘net base loss’, expressed as the difference between base loss and ammonia excretion, resulted in progressive reduction of arterial pH and [HCO3-]. The electrolyte status was also severely disturbed by progressively falling plasma [Na+] and [Cl-], which is attributed to failure of the active H+/Na+ and HCO3-/Cl- exchange mechanisms in the gills. At pHw 4.0 the acid-exposure syndrome is characterized by acid-base and electrolyte disturbances apparently not related to hypoxia. However, at pHw 3.5, tissue hypoxia, due to disturbances of gill gas exchange and to Bohr and Root effects, appears to be an additional important factor aggravating the disturbances of acid-base and electrolyte status.


1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.


1980 ◽  
Vol 84 (1) ◽  
pp. 289-302
Author(s):  
R. G. Boutilier ◽  
D. G. McDonald ◽  
D. P. Toews

A combined respiratory and metabolic acidosis occurs in the arterial blood immediately following 30 min of strenuous activity in the predominantly skin-breathing urodele, Cryptobranchus alleganiensis, and in the bimodal-breathing anuran, Bufo marinus, at 25 degrees C. In Bufo, the bulk of the post-exercise acidosis is metabolic in origin (principally lactic acid) and recovery is complete within 4-8 h. In the salamander, a lower magnitude, longer duration, metabolic acid component and a more pronounced respiratory acidosis prolong the recovery period for up to 22 h post-exercise. It is suggested that fundamental differences between the dominant sites for gas exchange (pulmonary versus cutaneous), and thus in the control of respiratory acid-base balance, may underline the dissimilar patterns of recovery from exercise in these two species.


1989 ◽  
Vol 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.


1991 ◽  
Vol 158 (1) ◽  
pp. 1-18 ◽  
Author(s):  
GEORGE K. IWAMA ◽  
NORBERT HEISLER

Acid-base regulation in rainbow trout acclimated to about 3, 100 and 500 mmol l−1 Na+ and Cl−, at constant water [HCO3−], was assessed during 24h of exposure to 1% CO2 and during recovery. The respiratory acidosis induced by a rise in plasma PCOCO2 to about 1.15kPa (8.5mmHg, 3mmol l−1), 1.33kPa (10mmHg, 100 mmol l−1) or 1.5 kPa (11.2 mmHg, 500 mmol l−1) was partially compensated for by accumulation of plasma HCO3−. The degree of pH compensation depended on the salinity of the environmental water, being about 61, 82 and 88% at 3, 100 and 300 mmol l−1 Na+ and Cl−, respectively. [HCO3−] in animals acclimated to 100 and 500 mmol l−1 rose to higher values than that in fish at 3 mmol l−1. Plasma [Cl−] decreased during hypercapnia as compared to control concentrations in all groups of fish. Plasma [Na+] rose during the first 8 h of hypercapnia in fish acclimated to all three salinities, but recovered towards control values during the remainder of hypercapnia. The rise in plasma [HCO3−] was significantly related to the fall in plasma [Cl−], whereas the changes in plasma [Na+] were unaffected by simultaneous changes in plasma [HCO3−]. Time courses of changes in plasma [Na+] and total ammonia concentration, [Tamm], were similar but in opposite directions. The transepithelial potential (TEP) of blood relative to water was negative, close to zero and positive, averaging −21, −5.8 and +6.2 mV for fish acclimated to 3, 100 and 300 mmol l−1 Na+, respectively. After initiation of hypercapnia, which caused a quite heterogeneous response among groups, a clear trend towards depolarization was observed during the remainder of hypercapnia. These results confirm the role of active HCO3−/Cl− exchange processes for the compensation of extracellular pH during respiratory acidoses in fish.


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