EXHAUSTIVE EXERCISE IN THE SEA LAMPREY (PETROMYZON MARINUS): RELATIONSHIP BETWEEN ANAEROBIC METABOLISM AND INTRACELLULAR ACID-BASE BALANCE

1993 ◽  
Vol 178 (1) ◽  
pp. 71-88 ◽  
Author(s):  
R. G. Boutilier ◽  
R. A. Ferguson ◽  
R. P. Henry ◽  
B. L. Tufts
Keyword(s):  
Respiratory Acidosis ◽  
High Energy ◽  
Exhaustive Exercise ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Change ◽  
Lactate Dehydrogenase Activity ◽  
Base Balance ◽  
Intracellular Acid

We measured intracellular acid-base balance and indicators of carbohydrate and high-energy phosphate metabolism as lampreys recovered from exhaustive exercise. A combined respiratory and metabolic acidosis was observed in the locomotory muscle following ‘burst’ exercise. Muscle pH decreased from approximately 7.2 to 6.7, whereas intracellular PCO2 rose from approximately 0.6 to 1.6 kPa. Unlike the situation in similarly stressed teleost fish such as rainbow trout, the respiratory acidosis in muscle persisted for several hours. This apparent CO2 retention in lamprey muscle may be the result of a restricted ability of the circulatory system to transport CO2 due to reduced erythrocyte anion exchange, or it could represent a restricted ability of the muscle itself to clear the intracellular pool of CO2 due to reduced carbonic anhydrase activity. Maximal lactate dehydrogenase activity of lamprey muscle exhibited a marked dependence on pH, increasing in activity by 30 % as pH decreased from 7.2 to 6.7 (reflecting the ‘resting’ to ‘post- exercise’ pH change observed in vivo). Following exhaustive exercise, the acid-base balance of the muscle is influenced by both proton- consuming (e.g. AMP deamination, glycogen replenishment) and proton-producing (e.g. rephosphorylation of creatine) metabolic processes. The net effect is that, although intracellular pH is maximally depressed, energy stores such as phosphocreatine and glycogen are partially restored within 1 h of exhaustive exercise, placing the animal in good stead for further locomotory work.

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

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.

Effect of systemic acid-base balance on ileal secretion

1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney
Keyword(s):  
Metabolic Acidosis ◽  
Cholera Toxin ◽  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Secretory Process ◽  
Sprague Dawley ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Change ◽  
Base Balance

We previously reported that systemic pH and HCO3 concentration affect ileal water and electrolyte absorption. To determine whether these effects could influence an ongoing secretory process, we measured transport in ileal loops exposed to either saline or 50-75 micrograms cholera toxin in mechanically ventilated Sprague-Dawley rats anesthetized with pentobarbital sodium. The effects of acute respiratory and metabolic acidosis and alkalosis were then examined. Decreases in systemic pH during respiratory acidosis caused equivalent increases in net water (54 +/- 8 microliters . cm-1 . h-1) and Na absorption (7 +/- 1 mu eq . cm- . h-1) and smaller increases in Cl absorption in cholera toxin compared with saline loops. These increases reversed the net secretion of these ions observed during alkalemia in the cholera toxin loops to net absorption. Metabolic acidosis and alkalosis and respiratory compensation of systemic pH of these metabolic disorders also altered cholera toxin-induced secretion in a direction consistent with the pH change. The increase in net HCO3 secretion caused by cholera toxin was unaffected by the respiratory disorders and did not vary with the HCO3 concentration in the metabolic disorders. These findings suggest that the systemic acid-base disorders that characterize intestinal secretory states may themselves alter intestinal absorptive function and fluid losses.

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus)

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman
Keyword(s):  
Plasma Osmolality ◽  
Respiratory Acidosis ◽  
Electrolyte Balance ◽  
Plasma Composition ◽  
Total Plasma ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Base Balance

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.

Effects of temperature on acid-base balance and ventilation in desert iguanas

1981 ◽  
Vol 51 (2) ◽  
pp. 452-460 ◽  
Author(s):  
P. E. Bickler
Keyword(s):  
Steady State ◽  
Pulmonary Ventilation ◽  
Respiratory Acidosis ◽  
Lung Ventilation ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Ph ◽  
Blood Relative ◽  
Base Balance ◽  
History Of

The effects of constant and changing temperatures on blood acid-base status and pulmonary ventilation were studied in the eurythermal lizard Dipsosaurus dorsalis. Constant temperatures between 18 and 42 degrees C maintained for 24 h or more produced arterial pH changes of -0.0145 U X degrees C-1. Arterial CO2 tension (PCO2) increased from 9.9 to 32 Torr plasma [HCO-3] and total CO2 contents remained constant at near 19 and 22 mM, respectively. Under constant temperature conditions, ventilation-gas exchange ratios (VE/MCO2 and VE/MO2) were inversely related to temperature and can adequately explain the changes in arterial PCO2 and pH. During warming and cooling between 25 and 42 degrees C arterial pH, PCO2 [HCO-3], and respiratory exchange ratios (MCO2/MO2) were similar to steady-state values. Warming and cooling each took about 2 h. During the temperature changes, rapid changes in lung ventilation following steady-state patterns were seen. Blood relative alkalinity changed slightly with steady-state or changing body temperatures, whereas calculated charge on protein histidine imidazole was closely conserved. Cooling to 17-18 degrees C resulted in a transient respiratory acidosis correlated with a decline in the ratio VE/MCO2. After 12-24 h at 17-18 degrees C, pH, PCO2, and VE returned to steady-state values. The importance of thermal history of patterns of acid-base regulation in reptiles is discussed.

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the aquatic gill-less urodele, Cryptobranchus alleganiensis; a comparison with the semi-terrestrial anuran, Bufo marinus

1980 ◽  
Vol 84 (1) ◽  
pp. 289-302
Author(s):  
R. G. Boutilier ◽  
D. G. McDonald ◽  
D. P. Toews
Keyword(s):  
Recovery Period ◽  
Respiratory Acidosis ◽  
Bufo Marinus ◽  
Acid Base Balance ◽  
Acid Base ◽  
Post Exercise ◽  
Arterial Blood ◽  
Cryptobranchus Alleganiensis ◽  
Base Balance ◽  
Lower Magnitude

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.

Regulation of urea synthesis by acid-base balance in vivo: role of NH3 concentration

1987 ◽  
Vol 252 (2) ◽  
pp. F221-F225 ◽  
Author(s):  
S. Cheema-Dhadli ◽  
R. L. Jungas ◽  
M. L. Halperin
Keyword(s):  
Ammonium Concentration ◽  
Urea Synthesis ◽  
Carbamoyl Phosphate ◽  
Acid Base Balance ◽  
Acid Base ◽  
Fixed Rate ◽  
Rate Limiting Step ◽  
Base Balance

The purpose of this study was to clarify how changes in acid-base balance influence the rate of urea synthesis in vivo. Since ureagenesis was increased by an ammonium infusion into rats, regulation seemed to be a function of the blood ammonium concentration. The rate of urea synthesis was constant at a fixed rate of ammonium infusion and independent of the conjugate base infused, chloride or bicarbonate. The steady-state blood ammonium concentration was higher in the rats that developed metabolic acidosis. Thus it appeared that regulation was not directly mediated by this ammonium concentration per se. The rate of urea synthesis was also independent of the blood pH. Accordingly, the rate of urea synthesis was examined as a function of the plasma NH3 concentration. The rate of ureagenesis was found to be directly proportional to the plasma NH3 concentration. Assuming that plasma NH3 levels reflect those in mitochondria, the NH3 concentration yielding half-maximal rates of urea synthesis (close to 2 microM) was in the same range as Km for the rate-limiting step in ureagenesis, carbamoyl phosphate synthetase (EC 6.3.4.16). These results suggest that, at a constant ammonium concentration, the decreased rate of ureagenesis caused by a pH fall in vitro could reflect an acidosis-induced decline in the concentration of true substrate (NH3) for this pathway.

scholarly journals Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

2007 ◽  
Vol 292 (3) ◽  
pp. G899-G904 ◽  
Author(s):  
Markus Sjöblom ◽  
Olof Nylander
Keyword(s):  
Base Excess ◽  
Ringer Solution ◽  
Bicarbonate Secretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
In Vivo Experiments ◽  
Arterial Blood ◽  
Blood Ph ◽  
Base Balance

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE2 was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15–7.21 and the base excess was about −8 mM at the end of experiments. The continuous infusion of Na2CO3 solution completely compensated for the acidosis. The blood pH was 7.36–7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE2-stimulated DMBS were markedly greater in animals treated with Na2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.

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