Distribution of H+ and HCO3 minus between CSF and blood during metabolic acidosis in dogs

To determine whether the regulation of brain extracellular fluid acid-base balance is by active ion transport or passive distribution, changes in cisternal and lumbar cerebrospinal fluid (CSF) (H+) and (HCO3 minus) were assessed in five dogs with normal acid-base status and in six dogs during metabolic acidosis. Both groups were mechanically ventilated to maintain a constant PaCO2. The pH, PCO2, (HCO3 minus), and (lactate) in CSF and arterial plasma and the CSF/plasma DC potential difference were determined at intervals, and the electrochemical potential differnces (mu) for H+ and HCO3 minus were calculated. Following control measurements at pHa equal to 7.40, metabolic acidosis was induced by infusion of 0.6 N HCl. Measurements were made 0, 3, 4.5, and 6 h thereafter and at 0, 3, and 6 h in the control series. A steady state for ion distribution was reached by 4.5 h. In the control series at 6 h the values of mu for H+ and HCO3 minus were within minus 0.2 and +0.5 mV of initial values at the cistern and +0.1 and +0.9 mV at the lumbar site. During metabolic acidosis, the 6-h values at the cistern returned to 0.0 and +0.7 mV of control for muH+ and muHCO3 minus while lumbar values returned to +0.5 and minus 0.4 mV. The closeness of these 6-h values of mu to control is compatible with passive distribution of H+ and HCO3 minus between CSF and blood.

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Extracellular Acid-Base Balance and Ion Transport Between Body Fluid Compartments

Physiology ◽

10.1152/physiol.00007.2017 ◽

2017 ◽

Vol 32 (5) ◽

pp. 367-379 ◽

Cited By ~ 9

Author(s):

Julian L. Seifter ◽

Hsin-Yun Chang

Keyword(s):

Ion Transport ◽

Ph Regulation ◽

Extracellular Fluid ◽

Transport Processes ◽

Electrolyte Balance ◽

Ph Homeostasis ◽

Acid Base Balance ◽

Acid Base ◽

Base Balance ◽

Fluid Compartments

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].

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ASSOCIATION OF ACID-BASE PARAMETERS WITH LACTATE LEVEL IN CRITICALLY ILL PATIENTS WITH METABOLIC ACIDOSIS

INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY ◽

10.24293/ijcpml.v24i2.1313 ◽

2018 ◽

Vol 24 (2) ◽

pp. 141

Author(s):

Donaliazarti Donaliazarti ◽

Rismawati Yaswir ◽

Hanifah Maani ◽

Efrida Efrida

Keyword(s):

Metabolic Acidosis ◽

Critically Ill ◽

Critically Ill Patients ◽

Lactate Level ◽

Linear Regression Analysis ◽

P Value ◽

Acid Base Balance ◽

Acid Base ◽

Base Parameters ◽

Base Balance

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.

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Distribution of H+ and HCO3 minus between CSF and blood during respiratory acidosis in dogs

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.228.4.1145 ◽

1975 ◽

Vol 228 (4) ◽

pp. 1145-1148 ◽

Cited By ~ 17

Author(s):

EG Pavlin ◽

TF Hornbein

Keyword(s):

Steady State ◽

Extracellular Fluid ◽

Respiratory Acidosis ◽

Potential Difference ◽

Ion Distribution ◽

Acid Base ◽

Mechanically Ventilated ◽

Brain Extracellular Fluid ◽

Dc Potential ◽

Arterial Plasma

To evaluate the regulation of (H+) and (HCO3 minus) in brain extracellular fluid during respiratory acidosis, the changes in cisternal and lumbar CSF acid-base state were assessed in six anteshetized, paralyzed, mechanically ventilated dogs rendered hypercapnic by increase in FIco2. Arterial (HCO3 minus) was held constant. The electrochemical potential difference (mu) between CSF and blood for H+ and HCO3 minus was calculated from values for (H+) and (HCO3 minus) in CSF and arterial plasma and the simultaneously measured CSF/plasma DC potential difference. Measurements were made at pHa equal to 7.40, after stable arterial values of pHa of about 7.2 were attained and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was attained by 4.5 h. Values of mu for H+ and HCO3 minus at 6 h had returned to +0.7 and minus 0.7 mV of control for cisternal CSF and +1.3 and minus 0.6 mV of control for lumbar CSF. The attainment of steady-state values for mu close to control is comparable with passive distribution of these ions between CSF and blood.

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Distribution of H+ and HCO3 minus between CSF and blood during metabolic alkalosis in dogs

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.228.4.1141 ◽

1975 ◽

Vol 228 (4) ◽

pp. 1141-1144 ◽

Cited By ~ 15

Author(s):

EG Pavlin ◽

ttf Hornbein

Keyword(s):

Cerebrospinal Fluid ◽

Steady State ◽

Metabolic Alkalosis ◽

Extracellular Fluid ◽

Ion Distribution ◽

Brain Extracellular Fluid ◽

Dc Potential ◽

Arterial Plasma ◽

Lumbar Cerebrospinal Fluid

In anesthetized, paralyzed dogs ventilated to maintain a normal PaCO2, metabolic alkalosis was induced and held constant over 6 h by infusion of sodium bicarbonate. Determination of pH, PCO2, (HCO3 minus), and (lactate) in cisternal and lumbar cerebrospinal fluid (CSF) and in arterial plasma together with measurement of the CSF/plasma DC potential differences permitted calculation of the electrochemical potential difference (mu) for H+ and HCO3 minus; measurements were made prior to induction of metabolic alkalosis at pHa equal to 7.40, as soon after induction as stable arterial values were achieved and 3, 4.5, and 6 h thereafter. A steady state for ion distribution was reached by 4.5 h. Values of mu for H+ and HCO3 minus returned to +0.1 and +0.9 mV of control at 6 h for cisternal CSF and +0.6 and minus 0.4 mV for lumbar CSF. This return of muH+ and muHCO3 minus close to control in the steady state is compatible with passive distribution of these ions between brain extracellular fluid and blood.

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Effect of systemic acid-base balance on ileal secretion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1987.253.3.g330 ◽

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.

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Effects of nutritionally induced metabolic acidosis with or without glutamine infusion on acid-base balance, plasma amino acids, and plasma nonesterified fatty acids in sheep1

Journal of Animal Science ◽

10.2527/jas.2008-1165 ◽

2009 ◽

Vol 87 (3) ◽

pp. 1077-1084 ◽

Cited By ~ 3

Author(s):

N. E. Odongo ◽

S. L. Greenwood ◽

M. M. Or-Rashid ◽

D. Radford ◽

O. AlZahal ◽

...

Keyword(s):

Amino Acids ◽

Fatty Acids ◽

Metabolic Acidosis ◽

Plasma Amino Acids ◽

Acid Base Balance ◽

Acid Base ◽

Nonesterified Fatty Acids ◽

Base Balance

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Chronic metabolic acidosis upregulates rat kidney Na-HCO 3 − cotransporters NBCn1 and NBC3 but not NBC1

AJP Renal Physiology ◽

10.1152/ajprenal.00104.2001 ◽

2002 ◽

Vol 282 (2) ◽

pp. F341-F351 ◽

Cited By ~ 77

Author(s):

Tae-Hwan Kwon ◽

Christiaan Fulton ◽

Weidong Wang ◽

Ira Kurtz ◽

Jørgen Frøkiær ◽

...

Keyword(s):

Metabolic Acidosis ◽

Rat Kidney ◽

Free Access ◽

Thick Ascending Limb ◽

Acid Base Balance ◽

Acid Base ◽

Chronic Metabolic Acidosis ◽

Daily Water Intake ◽

Base Balance ◽

Access To Water

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].

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