scholarly journals Switch from Metabolic to Ventilatory Compensation of Extracellular pH in Crayfish

1988 ◽  
Vol 137 (1) ◽  
pp. 411-420 ◽  
Author(s):  
B. Burtin ◽  
J.-C. Massabuau

The mechanisms of extracellular pH regulation were studied in crayfish Astacus leptodactylus under conditions that were either favourable or unfavourable for ionoregulation. Animals in intermoult or premoult stages were kept in normoxic artificial waters at 13°C. In intermoult, acid—base balance (ABB) and ionoregulatory disturbances were induced by increasing the ambient partial pressure of CO2 (PwCOCO2), by decreasing the concentration of NaCl in the water ([NaCl]w) or by associating both changes. In premoult we took advantage of the spontaneously occurring endogenous problems of ionoregulation which are linked to shell shedding. In intermoult, an increase of PwCOCO2 alone induced a hypercapnic acidosis compensated by metabolic means, whereas in association with a decrease of [NaCl]w (which induced a decrease of [NaCl] in the haemolymph) it led to a ventilatory compensation. In intermoult a decrease of [NaCl]w alone induced a metabolic acidosis that was compensated by metabolic means, whereas in premoult it was compensated by ventilatory adjustments. It is concluded that when water breathers are facing experimentally induced or spontaneous ionoregulatory problems, compensation for superimposed ABB disturbances can be made by ventilatory adjustments instead of by metabolic means.

Physiology ◽  
2017 ◽  
Vol 32 (5) ◽  
pp. 367-379 ◽  
Author(s):  
Julian L. Seifter ◽  
Hsin-Yun Chang

Clinical assessment of acid-base disorders depends on measurements made in the blood, part of the extracellular compartment. Yet much of the metabolic importance of these disorders concerns intracellular events. Intracellular and interstitial compartment acid-base balance is complex and heterogeneous. This review considers the determinants of the extracellular fluid pH related to the ion transport processes at the interface of cells and the interstitial fluid, and between epithelial cells lining the transcellular contents of the gastrointestinal and urinary tracts that open to the external environment. The generation of acid-base disorders and the associated disruption of electrolyte balance are considered in the context of these membrane transporters. This review suggests a process of internal and external balance for pH regulation, similar to that of potassium. The role of secretory gastrointestinal epithelia and renal epithelia with respect to normal pH homeostasis and clinical disorders are considered. Electroneutrality of electrolytes in the ECF is discussed in the context of reciprocal changes in Cl−or non Cl−anions and [Formula: see text].


Author(s):  
Donaliazarti Donaliazarti ◽  
Rismawati Yaswir ◽  
Hanifah Maani ◽  
Efrida Efrida

Metabolic acidosis is prevalent among critically ill patients and the common cause of metabolic acidosis in ICU is lactic acidosis. However, not all ICUs can provide lactate measurement. The traditional method that uses Henderson-Hasselbach equation (completed with BE and AG) and alternative method consisting of Stewart and its modification (BDEgap and SIG), are acid-base balance parameters commonly used by clinicians to determine metabolic acidosis in critically ill patients. The objective of this study was to discover the association between acid-base parameters (BE, AGobserved, AGcalculated, SIG, BDEgap) with lactate level in critically ill patients with metabolic acidosis. This was an analytical study with a cross-sectional design. Eighty-four critically ill patients hospitalized in the ICU department Dr. M. Djamil Padang Hospital were recruited in this study from January to September 2016. Blood gas analysis and lactate measurement were performed by potentiometric and amperometric method while electrolytes and albumin measurement were done by ISE and colorimetric method (BCG). Linear regression analysis was used to evaluate the association between acid-base parameters with lactate level based on p-value less than 0.05. Fourty five (54%) were females and thirty-nine (46%) were males with participant’s ages ranged from 18 to 81 years old. Postoperative was the most reason for ICU admission (88%). Linear regression analysis showed that p-value for BE, AGobserved, AGcalculated, SIG and BDEgap were 119; 0.967; 0.001; 0.001; 0.689, respectively. Acid-base balance parameters which were mostly associated with lactate level in critically ill patients with metabolic acidosis were AGcalculated and SIG. 


1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney

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.


2002 ◽  
Vol 282 (2) ◽  
pp. F341-F351 ◽  
Author(s):  
Tae-Hwan Kwon ◽  
Christiaan Fulton ◽  
Weidong Wang ◽  
Ira Kurtz ◽  
Jørgen Frøkiær ◽  
...  

Several members of the Na-HCO[Formula: see text] cotransporter (NBC) family have recently been identified functionally and partly characterized, including rkNBC1, NBCn1, and NBC3. Regulation of these NBCs may play a role in the maintenance of intracellular pH and in the regulation of renal acid-base balance. However, it is unknown whether the expressions of these NBCs are regulated in response to changes in acid-base status. We therefore tested whether chronic metabolic acidosis (CMA) affects the abundance of these NBCs in kidneys using two conventional protocols. In protocol 1, rats were treated with NH4Cl in their drinking water (12 ± 1 mmol · rat−1 · day−1) for 2 wk with free access to water ( n = 8). Semiquantitative immunoblotting demonstrated that whole kidney abundance of NBCn1 and NBC3 in rats with CMA was dramatically increased to 995 ± 87 and 224 ± 35%, respectively, of control levels ( P < 0.05), whereas whole kidney rkNBC1 was unchanged (88 ± 14%). In protocol 2, rats were given NH4Cl in their food (10 ± 1 mmol · rat−1 · day−1) for 7 days, with a fixed daily water intake ( n = 6). Consistent with protocol 1, whole kidney abundances of NBCn1 (262 ± 42%) and NBC3 (160 ± 31%) were significantly increased compared with controls ( n = 6), whereas whole kidney rkNBC1 was unchanged (84 ± 17%). In both protocols, immunocytochemistry confirmed upregulation of NBCn1 and NBC3 with no change in the segmental distribution along the nephron. Consistent with the increase in NBCn1, measurements of pH transients in medullary thick ascending limb (mTAL) cells in kidney slices revealed two- to threefold increases in DIDS- sensitive, Na+-dependent HCO[Formula: see text] uptake in rats with CMA. In conclusion, CMA is associated with a marked increase in the abundance of NBCn1 in the mTAL and NBC3 in intercalated cells, whereas the abundance of NBC1 in the proximal tubule was not altered. The increased abundance of NBCn1 may play a role in the reabsorption of NH[Formula: see text] in the mTAL and increased NBC3 in reabsorbing HCO[Formula: see text].


2010 ◽  
Vol 30 (5) ◽  
pp. 63-69 ◽  
Author(s):  
Melissa Beaudet Jones

What are the basic concepts of acid-base balance, the 2 types of metabolic acidosis, and the common causes of each type of metabolic acidosis?


Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 899 ◽  
Author(s):  
Holger M. Becker ◽  
Joachim W. Deitmer

Solid tumors are metabolically highly active tissues, which produce large amounts of acid. The acid/base balance in tumor cells is regulated by the concerted interplay between a variety of membrane transporters and carbonic anhydrases (CAs), which cooperate to produce an alkaline intracellular, and an acidic extracellular, environment, in which cancer cells can outcompete their adjacent host cells. Many acid/base transporters form a structural and functional complex with CAs, coined “transport metabolon”. Transport metabolons with bicarbonate transporters require the binding of CA to the transporter and CA enzymatic activity. In cancer cells, these bicarbonate transport metabolons have been attributed a role in pH regulation and cell migration. Another type of transport metabolon is formed between CAs and monocarboxylate transporters, which mediate proton-coupled lactate transport across the cell membrane. In this complex, CAs function as “proton antenna” for the transporter, which mediate the rapid exchange of protons between the transporter and the surroundings. These transport metabolons do not require CA catalytic activity, and support the rapid efflux of lactate and protons from hypoxic cancer cells to allow sustained glycolytic activity and cell proliferation. Due to their prominent role in tumor acid/base regulation and metabolism, transport metabolons might be promising drug targets for new approaches in cancer therapy.


Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1913 ◽  
Author(s):  
Tianying Wu ◽  
Phoebe Seaver ◽  
Hector Lemus ◽  
Kathryn Hollenbach ◽  
Emily Wang ◽  
...  

Metabolic acidosis can lead to inflammation, tissue damage, and cancer metastasis. Dietary acid load contributes to metabolic acidosis if endogenous acid–base balance is not properly regulated. Breast cancer survivors have reduced capacities to adjust their acid–base balance; yet, the associations between dietary acid load and inflammation and hyperglycemia have not been examined among them. We analyzed data collected from 3042 breast cancer survivors enrolled in the Women’s Healthy Eating and Living (WHEL) Study who had provided detailed dietary intakes and measurements of plasma C-reactive protein (CRP) and hemoglobin A1c (HbA1c). Using a cross-sectional design, we found positive associations between dietary acid load and plasma CRP and HbA1c. In the multivariable-adjusted models, compared to women with the lowest quartile, the intakes of dietary acid load among women with the highest quartile showed 30–33% increases of CRP and 6–9% increases of HbA1c. Our study is the first to demonstrate positive associations between dietary acid load and CRP and HbA1c in breast cancer survivors. Our study identifies a novel dietary factor that may lead to inflammation and hyperglycemia, both of which are strong risk factors for breast cancer recurrence and comorbidities.


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