Role of skeletal muscle in plasma ion and acid-base regulation after NaHCO3 and KHCO3 loading in humans

1999 ◽  
Vol 276 (1) ◽  
pp. R32-R43 ◽  
Author(s):  
Michael I. Lindinger ◽  
Thomas W. Franklin ◽  
Larry C. Lands ◽  
Preben K. Pedersen ◽  
Donald G. Welsh ◽  
...  

This paper examines the time course of changes in plasma electrolyte and acid-base composition in response to NaHCO3 and KHCO3 ingestion. It was hypothesized that skeletal muscle is involved in the correction of the ensuing plasma disturbance by exchanging ions, gasses, and fluids between cells and extracellular fluids. Five male subjects, with catheters in a brachial artery and antecubital vein, ingested 3.57 mmol/kg body mass NaHCO3 or KHCO3. While seated, blood samples were taken 30 min before ingestion of the solution, at 10-min intervals during the 60-min ingestion period, and periodically for 210 min after ingestion was complete. Blood was analyzed for gases, hematocrit, plasma ions, and total protein. With NaHCO3, arterial plasma Na+ concentration ([Na+]) increased from 143 ± 1 to 147 ± 1 (SE) meq/l, H+ concentration ([H+]) decreased by 6 ± 1 neq/l, and [Formula: see text] increased by 5 ± 1 mmHg. There was no detectable net Na+ uptake by tissues. An increased plasma strong ion difference ([SID]) accounted fully for the decrease in plasma [H+]. With KHCO3, K+ concentration increased from 4.25 ± 0.10 to 7.17 ± 0.13 meq/l, plasma volume decreased by 15.5 ± 2.3%, [H+] decreased by 4 ± 1 neq/l, and there was no change in[Formula: see text]. The decrease in [H+] in the KHCO3 trial primarily arose in response to the increased [SID]. Net K+ uptake by tissues accounted for 37 ± 5% of the ingested K+. In conclusion, ingestion of NaHCO3and KHCO3 produced markedly different fluid and ionic disturbances and associated regulatory responses by skeletal muscle. Accordingly, the physicochemical origins of the acid-base disturbances also differed between treatments. The tissues did not play a role in regulating plasma [Na+] after ingestion of NaHCO3. In contrast, the net influx of K+ to tissues played an important role in removing K+ from the extracellular compartment after ingestion of KHCO3.

2006 ◽  
Vol 3 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger

AbstractMeasurement and interpretation of acid–base status are important in clinical practice and among racing jurisdictions to determine if horses have been administered alkalinizing substances for the purpose of enhancing performance. The present study used the physicochemical approach to characterize the daily variation in plasma electrolytes and acid–base state that occurs in horses in the absence of feeding and exercise. Jugular venous blood was sampled every 1–2 h from two groups (n=4 and n=5) of Standardbred horses over a 25 h period where food and exercise were withheld. One group of horses was studied in October and one in December. The time course and magnitude of circadian responses differed between the two groups, suggesting that subtle differences in environment may manifest in acid–base status. Significant daily variation occurred in plasma weak acid concentration ([Atot]) and strong ion difference ([SID]), [Cl−], [K+], [Na+] and [lactate−], which contributed to significant changes in [H+] and TCO2. The night-time period was associated with a mild acidosis, marked by increases in plasma [H+] and decreases in TCO2, compared with the morning hours. The night-time acidosis resulted from an increased plasma [Atot] due to an increased plasma protein concentration ([PP]), and a decreased [SID] due to increases in [Cl−] and decreases in [Na+]. An increased plasma [K+] during the night-time had a mild alkalotic effect. There were no differences in pCO2. It was concluded that many equine plasma electrolyte and acid–base parameters exhibit fluctuations in the absence of feeding and exercise, and it is likely that some of these changes are due to daily variation.


1983 ◽  
Vol 107 (1) ◽  
pp. 9-20 ◽  
Author(s):  
D. P. Toews ◽  
G. F. Holeton ◽  
N. Heisler

Specimens of Conger conger (L.) were exposed to environmental hypercapnia in a closed recirculating seawater system. Arterial plasma pH, PCO2 and bicarbonate concentration, as well as the net transfer of bicarbonate and ammonia between fish and ambient seawater, were monitored for 30 h of hypercapnia. The initial hypercapnia-induced reduction of arterial pH by about 0.4 pH units was restored to near control values within 10 h of hypercapnia by compensatory elevation of plasma bicarbonate concentration. The continuous rise in extracellular bicarbonate from about 5 to 22 mM during this time was the result of two different mechanisms. Initially, there was a net bicarbonate transfer from the intracellular space to the extracellular compartment until the net uptake of bicarbonate from the seawater started. The amount of bicarbonate originally transferred to the extracellular space was then returned to the intracellular compartment and finally the changes in both extracellular and intracellular pH were compensated by bicarbonate taken up from the environmental seawater. Since the ammonia excretion was not increased during hypercapnia and the pattern of plasma electrolyte concentrations does not favour the H+/Na+ ion exchange mechanism, it is concluded that the additional bicarbonate is gained by active HCO3-/Cl- ion exchange against the electrochemical gradient between fish and seawater.


1994 ◽  
Vol 76 (3) ◽  
pp. 1211-1219 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)


1959 ◽  
Vol 196 (2) ◽  
pp. 283-286 ◽  
Author(s):  
W. W. Swingle ◽  
J. P. DaVanzo ◽  
D. Glenister ◽  
H. C. Crossfield ◽  
G. Wagle

Daily doses (5 mg) of 1-dehydrohydrocortisone reduces plasma Na and Cl of nonfasted adrenalectomized dogs to levels characteristic of severe insufficiency. The animals remain active and vigorous despite the distorted plasma electrolyte pattern. Blood pressure and plasma volume remain at or near control values. The glucocorticoid maintains a normal internal distribution of fluid and certain electrolytes between intra- and extracellular compartments. Aldosterone even in large doses apparently lacks those properties necessary to enable the fasted adrenalectomized dog exhibiting symptoms to shift fluids from one compartment to another hence is incapable of reviving animals from insufficiency and restoring activity and vigor. The data suggest that the primary action of aldosterone is on the kidney and through renal control of Na excretion serves to regulate the fluid and Na content of the extracellular compartment.


2002 ◽  
Vol 283 (6) ◽  
pp. E1272-E1278 ◽  
Author(s):  
Adam Steensberg ◽  
Charlotte Keller ◽  
Rebecca L. Starkie ◽  
Takuya Osada ◽  
Mark A. Febbraio ◽  
...  

The aim of the present study was to examine whether IL-6 and TNF-α are expressed in, and released from, human skeletal muscle during exercise. We hypothesized that the skeletal muscle will release IL-6, but not TNF-α, during exercise because of previous observations that TNF-α negatively affects glucose uptake in skeletal muscle. Six healthy, male subjects performed 180 min of two-legged knee-extensor exercise. Muscle samples were obtained from the vastus lateralis of one limb. In addition, blood samples were obtained from a femoral artery and vein. Plasma was analyzed for IL-6 and TNF-α. We detected both IL-6 and TNF-α mRNA in resting muscle samples, and whereas IL-6 increased ( P < 0.05) ∼100-fold throughout exercise, no significant increase in TNF-α mRNA was observed. Arterial plasma TNF-α did not increase during exercise. Furthermore, there was no net release of TNF-α either before or during exercise. In contrast, IL-6 increased throughout exercise in arterial plasma, and a net IL-6 release from the contracting limb was observed after 120 min of exercise ( P < 0.05).


1983 ◽  
Vol 54 (1) ◽  
pp. 3-12 ◽  
Author(s):  
E. E. Nattie

This review emphasizes the importance of strong ions in the regulation of cerebrospinal fluid (CSF) acid-base balance. In a solution like CSF that is devoid of nonbicarbonate buffers. [H+] and [HCO-3] are dependent variables, the independent variables being the CO2 partial pressure (PCO2) and the strong ion difference. Any measureable changes in CSF [HCO-3] and any change in [H+] that occur independent of changes in PCO2 must be accompanied by, if not caused by, changes in strong ions. The role of H+ and HCO-3 vs. strong ions in the ionic mechanisms of CSF acid-base regulation is unknown. For example, these mechanisms could depend only on changes in strong ions that accompany acid-base disorders, or they could be triggered by changes in [H+] or PCO2. These ideas are presented within the context of current concepts concerning the relationship of CSF to brain interstitial fluid (ISF) and the importance of choroid plexus and blood-brain barrier mechanisms in determining CSF and ISF ionic composition. Studies concerning CSF strong ions in normal and abnormal acid-base states are reviewed.


1999 ◽  
Vol 86 (5) ◽  
pp. 1617-1625 ◽  
Author(s):  
V. Alfaro ◽  
J. Pesquero ◽  
L. Palacios

The present study tests the hypothesis that changes in the strong inorganic ion concentrations contribute significantly to the acid-base disturbance that develops during hemorrhage in the arterial plasma of rats in addition to lactate concentration ([Lac−]) increase. The physicochemical origins for this acid-base disorder were studied during acute, graded hemorrhage (10, 20, and 30% loss of blood volume) in three groups of rats: conscious, anesthetized with ketamine, and anesthetized with urethan. The results support the hypothesis examined: strong-ion difference (SID) decreased in the arterial plasma of all groups studied because of an early imbalance in the main strong inorganic ions during initial hemorrhagic phase. Moreover, changes in plasma [Lac−] contributed to SID decrease in a later hemorrhagic phase (after 10% hemorrhage in urethan-anesthetized, after 20% hemorrhage in ketamine-anesthetized, and after 30% hemorrhage in conscious group). Inorganic ion changes were due to both dilution of the vascular compartment and ion exchange with extravascular space and red blood cells, as compensation for blood volume depletion and hypocapnia. Nevertheless, anesthetized rats were less able than conscious rats to preserve normal arterial pH during hemorrhage, mainly because of an impaired peripheral tissue condition and incomplete ventilatory compensation.


2005 ◽  
Vol 2 (3) ◽  
pp. 159-169 ◽  
Author(s):  
Amanda Waller ◽  
Kerri Jo Smithurst ◽  
Gayle L Ecker ◽  
Ray Geor ◽  
Michael I Lindinger

AbstractThe present study used the physicochemical approach to characterize the changes in plasma electrolyte and acid–base states that occur in horses in response to feeding. Jugular venous blood was sampled every 0.5–2 h over a 24-h period from two groups (n = 4 and n = 5) of Standardbreds fed a mixed hay and grain ration at 8 am and 7 pm. One group of horses was studied in October, and one in December. The time course and magnitude of feeding responses differed between groups, and between the morning and evening meals. Feeding-induced changes in plasma electrolyte and acid–base variables occurred rapidly, within the first 1–3 h of meal consumption. The plasma acidosis associated with eating the meal was marked by increased plasma [H+] and decreased TCO2. The primary contributors to the increases in plasma [H+] were the decrease in the plasma concentration of strong ions ([SID]) and the pCO2. The increase in plasma total weak acid (protein) concentration ([Atot]) post-feeding had only a minor effect on the acid–base state. The feeding-induced acidosis abated 3–6 h after the meal, showing cyclical recovery of physicochemical variables that contributed to the acid–base disturbance. It is concluded that several key plasma electrolyte and acid–base parameters undergo significant, cyclical fluctuations in response to feeding in horses.


1986 ◽  
Vol 121 (1) ◽  
pp. 77-94 ◽  
Author(s):  
P. R. H. WILKES ◽  
B. R. MCMAHON

The effects of exposure to 0.94% (300 mosmol1−1) sodium chloride on plasma electrolyte and acid-base status were examined in the freshwater stenohaline teleost Catostomus commersoni (Lacépède), the white sucker. Four days' exposure to this maximum sublethal salinity resulted in an increase in plasma concentrations of both sodium and chloride but a decrease in the Na+/Cl− ratio. Since the plasma concentrations of free amino acids and other strong ions - Ca2+, Mg2+ and K+ - remained unchanged, plasma strong ion difference (SID) decreased. Additionally, plasma pH and bicarbonate concentration decreased at constant Pcoco2 The changes in electrolyte and acid-base status that occurred after the 96 h were not appreciably altered after a further 2–3 weeks of saline exposure. The ambient calcium concentration had no influence on these results. Haemolymph non-bicarbonate buffer capacity (β) calculated as Δ[HCO3−]/ ΔpH, increased in saline-exposed fish. Consequently ΔH+, the apparent proton load, was zero despite the apparent change in acid-base status. Although β was directly proportional to the haemoglobin concentration in both control and experimental fish, this could not account for the increase in β since haemoglobin remained at control values. These results can be explained solely by the change in plasma SID and serve to illustrate the dependence of plasma acid-base status on the prevailing electrolyte characteristics, weak acid concentration and Pcoco2.


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