Isolated perfused head of rainbow trout. I. Gas transfer, acid-base balance, and hemodynamics

1985 ◽  
Vol 249 (2) ◽  
pp. R246-R254 ◽  
Author(s):  
S. F. Perry ◽  
C. E. Booth ◽  
D. G. McDonald
Keyword(s):  
Carbonic Anhydrase ◽  
Blood Perfusion ◽  
Aortic Pressure ◽  
Gas Transfer ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Gradients ◽  
Base Balance ◽  
Co2 Excretion

Branchial gas transfer, acid-base balance, and hemodynamics were critically evaluated and compared in Ringer-perfused and blood-perfused heads of rainbow trout. Blood perfusion stimulated O2 uptake and CO2 excretion across the gills to values more representative of intact fish. The stimulatory effect of blood on gas transfer was due to increased O2 carrying capacity (O2 uptake) and the presence of erythrocytic carbonic anhydrase (CO2 excretion). Adding carbonic anhydrase to Ringer enhanced CO2 excretion in a manner similar to blood. During Ringer perfusion, arteriovenous pH gradients were abnormal (arterial pH less than venous pH). Perfusion with blood or addition of carbonic anhydrase to Ringer reversed the pH gradients to typical in vivo levels. Branchial vascular resistance to flow was abnormally high in both Ringer- and blood-perfused preparations, primarily as a result of low dorsal aortic pressure. Input pressure increased during blood perfusion and was similar to ventral aortic pressure in vivo. Perfusion with Ringer may have caused irreversible deterioration of gill function as indicated by decreased arterial Po2 and O2 extraction effectiveness after a rapid switch from Ringer to blood perfusion. The results are discussed with reference to the suitability of perfused trout head preparations for studying gill gas transfer, acid-base balance, and hemodynamics. Comparisons are made between the perfused head preparation and intact fish as well as with other types of perfused gill preparations.

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.

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.

scholarly journals A role for bicarbonate in the regulation of mammalian glutamine metabolism

1979 ◽  
Vol 184 (3) ◽  
pp. 599-606 ◽  
Author(s):  
G Baverel ◽  
P Lund
Keyword(s):  
Rat Kidney ◽  
Glutamine Metabolism ◽  
Kidney Cortex ◽  
Complete Oxidation ◽  
Kidney Tubules ◽  
Acid Base Balance ◽  
Acid Base ◽  
Rat Kidney Cortex ◽  
Base Balance

1. The concentration of HCO3- (independent of any change of pH) exerts different effects on glutamine metabolism in rat kidney-cortex tubules, hepatocytes and enterocytes.2. In kidney tubules HCO3- (10.5-50 MM) has no effect on glutaminase (EC 3.5.1.2), whereas glutamate dehydrogenase (EC 1.4.1.3) is inhibited as HCO3- concentration is increased. The result is that flux through the entire glutamate-to-glucose pathway is inhibited by increasing HCO3- concentrations. A large proportion (more than 30%) of the glutamine removed undergoes complete oxidation. 3. In hepatocytes, and to a smaller extent in enterocytes, HCO3- is an accelerator of glutaminase. Synthesis of glucose and urea from glutamine in hepatocytes increases as HCO3- concentration is increased. Calculations show that fumarate, formed via aspartate aminotransferase and arginino-succinate lyase, is the precursor of the glucose. There is no complete oxidation of the carbon skeleton of glutamine in hepatocytes. 4. Leucine at near-physiological concentrations (0.1-1 mM) is an accelerator of glutaminase in hepatocytes, but not in kidney tubules or in enterocytes. 5. The results are discussed in relation to regulation of acid/base balance in vivo.

scholarly journals Haemolymph Acid-Base, Electrolyte and Gas Status during Sustained Voluntary Activity in the Land Hermit Crab (Coenobita Compressus)

1986 ◽  
Vol 125 (1) ◽  
pp. 225-243
Author(s):  
Michéle G. Wheatly ◽  
Brian R. Mcmahon ◽  
Warren W. Burggren ◽  
Alan W. Pinder
Keyword(s):  
Hermit Crab ◽  
Oxygen Binding ◽  
Acid Base Balance ◽  
Acid Base ◽  
Voluntary Activity ◽  
Binding Characteristics ◽  
Base Balance ◽  
External Water ◽  
O2 Delivery

After 3h(50 m) of voluntary walking, the haemolymph pH of the land hermit crab Coenobita compressus (H. Milne Edwards) decreased by 0.4units. This was accompanied by increases in CO2 tension (Pcoco2). bicarbonate (HCO3− + CO32-) and lactate concentrations. The hypercapnic acidosis was partially compensated by metabolic bicarbonate accumulation and an H+ deficit developed. Unloaded crabs accumulated less of a proton load than crabs transporting mollusc shells. During activity, oxygenation of the haemocyanin (HCy) accounted for the release of 0.3 mmol CO2l−1, via the Haldane effect, which was seven times more than in settled crabs. Control acid-base balance was re-established within 1 h of recovery. At this time, acidic equivalents were excreted at a mean flux rate of 5 mequiv kg−1 h−1 into a source of external water. [Na+] and the ratio of [Na+]:[Cl−] increased during exercise. Coenobita haemolymph had a high O2-carrying capacity (CmaxHCyOHCyO2 = l.55 mmol 1−1). HCy oxygen-binding characteristics were typical of other decapods (φ= −0.44), yet no lactate sensitivity was apparent. Settled in vivo values of O2 tension (Poo2) and content (Coo2) were located around the half-saturation tension (P50) of the dissociation curve. During exercise, POO2 increased and an unopposed Bohr shift decreased the O2-binding affinity, thereby reducing postbranchial saturation. Quantitatively, however, compensations in cardiac output (V·b) were more instrumental in increasing the O2 delivery to respiring tissues. During recovery, haemolymph POO2 remained high and the venous reserve doubled.

scholarly journals Expression patterns of two Carbonic anhydrase genes, Na+/K+-ATPase and V-type H+-ATPase in the freshwater crayfish, Cherax quadricarinatus, under different pH

2015 ◽  
Author(s):  
Muhammad Yousuf Ali ◽  
Ana Pavasovic ◽  
Peter B Mather ◽  
Peter J Prentis
Keyword(s):  
Carbonic Anhydrase ◽  
Expression Patterns ◽  
Low Ph ◽  
Freshwater Crayfish ◽  
Acid Base Balance ◽  
Acid Base ◽  
Expression Levels ◽  
High Ph ◽  
Base Balance ◽  
Ph Conditions

Osmoregulation and systemic acid-base balance in decapod crustaceans are largely controlled by a set of transport-related enzymes including carbonic anhydrase (CA), Na + /K + -ATPase (NKA) and V-type- H + -ATPase (HAT). Variable pH levels and changes in osmotic pressure can have a significant impact on the physiology and behaviour of crustaceans. Therefore, it is crucial to understand the mechanisms via which an animal can maintain its internal pH balance and regulate the movement of ions into and out of its cells. Here, we examined expression patterns of the cytoplasmic (CAc) and membrane-associated form (CAg) of CA, NKA α subunit and HAT subunit a in gills of the freshwater crayfish Cherax quadricarinatus. Expression levels of the genes were measured at three pH levels, pH 6.2, 7.2 (control) and 8.2 over a 24 hour period. All genes showed significant differences in expression levels, either among pH treatments or over time. Expression levels of CAc were significantly increased at low pH and decreased at high pH conditions 24 h after transfer to these treatments. Expression increased in low pH after 12 h, and reached their maximum level by 24 h. The membrane-associated form CAg showed changes in expression levels more quickly than CAc. Expression increased for CAg at 6 h post transfer at both low and high pH conditions, but expression remained elevated only at low pH (6.2) at the end of the experiment. Expression of CqNKA significantly increased at 6 h after transfer to pH 6.2 and remained elevated up to 24 h. Expression for HAT and NKA showed similar patterns, where expression significantly increased 6 h post transfer to the low pH conditions and remained significantly elevated throughout the experiment. The only difference in expression between the two genes was that HAT expression decreased significantly 24 h post transfer to high pH conditions. Overall, our data suggest that CAc, CAg, NKA and HAT gene expression is induced at low pH conditions in freshwater crayfish. Further research should examine the physiological underpinnings of these changes in expression to better understand systemic acid/base balance in freshwater crayfish.

Renal regulation of acid-base balance in the bullfrog

1961 ◽  
Vol 201 (6) ◽  
pp. 980-986 ◽  
Author(s):  
Hisato Yoshimura ◽  
Masateru Yata ◽  
Minoru Yuasa ◽  
Robert A. Wolbach
Keyword(s):  
Carbonic Anhydrase ◽  
Ammonia Excretion ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urinary Ph ◽  
Base Balance ◽  
Chloride Excretion ◽  
Acid Load ◽  
Renal Carbonic Anhydrase

Renal mechanisms for the maintenance of acid-base balance were studied in the normal bullfrog, during metabolic and respiratory acidosis, and after carbonic anhydrase inhibition. Following intravenous administration of 0.3–12 mmole HCl/ kg, as 0.1 n HCl, urinary pH (initially pH 6.3–7.7) did not change significantly. However, urinary ammonia excretion increased more than twofold, and within 3–5 days the cumulative increase was equivalent to the acid load given. Despite the increased ammonia excretion, chloride excretion did not increase after acid loading. In both normal and acidotic bullfrogs ammonia excretion was correlated with an increase in urinary pH. Respiratory acidosis in the small frog, Rana limnocharis, produced by exposure to 6.4% CO2 in air, induced neither urinary acidification nor increased ammonia excretion; both urinary sodium and bicarbonate excretion increased. When renal carbonic anhydrase was inhibited by acetazoleamide injection, urine flow, sodium excretion, and bicarbonate excretion increased markedly, urinary pH increased slightly, and urinary ammonia excretion remained unchanged. These renal responses to acidosis are compared with those of the acidotic dog.

Is urea formation regulated primarily by acid-base balance in vivo?

1986 ◽  
Vol 250 (4) ◽  
pp. F605-F612 ◽  
Author(s):  
M. L. Halperin ◽  
C. B. Chen ◽  
S. Cheema-Dhadli ◽  
M. L. West ◽  
R. L. Jungas
Keyword(s):  
Dietary Protein ◽  
Urea Synthesis ◽  
Acid Base Balance ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Wide Range ◽  
Base Balance ◽  
Acid Load ◽  
Acid Base Status

Large quantities of ammonium and bicarbonate are produced each day from the metabolism of dietary protein. It has recently been proposed that urea synthesis is regulated by the need to remove this large load of bicarbonate. The purpose of these experiments was to test whether the primary function of ureagenesis in vivo is to remove ammonium or bicarbonate. The first series of rats were given a constant acid load as hydrochloric acid or ammonium chloride; individual rats received a constant nitrogen load at a time when their plasma acid-base status ranged from normal (pH 7.4, 28 mM HCO3) to severe metabolic acidosis (pH 6.9, 6 mM HCO3). Urea plus ammonium excretions and the blood urea, glutamine, and ammonium concentrations were monitored with time. Within the constraints of non-steady-state conditions, the rate of urea synthesis was constant and the plasma glutamine and ammonium concentrations also remained constant; thus it appears that the rate of urea synthesis was not primarily regulated by the acid-base status of the animal in vivo over a wide range of plasma ammonium concentrations. In quantitative terms, the vast bulk of the ammonium load was converted to urea over 80 min; only a small quantity of ammonium appeared as circulating glutamine or urinary ammonium. Urea synthesis was proportional to the nitrogen load. A second series of rats received sodium bicarbonate; urea synthesis was not augmented by a bicarbonate load. We conclude from these studies that the need to dispose of excess bicarbonate does not primarily determine the rate of ureagenesis in vivo. The data support the classical view that ureagenesis is controlled by the quantity of ammonium to be removed.

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