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PubMed2002

Importance of hypoxic vasoconstriction in maintaining oxygenation during acute lung injury.

OBJECTIVE: To investigate the role of hypoxic pulmonary vasoconstriction in the intrapulmonary blood flow redistribution and gas exchange protection during oleic acid acute lung injury. DESIGN: Prospective, controlled animal study. SETTING: Research laboratory of an academic institution. SUBJECTS: Three groups of five mongrel dogs. INTERVENTIONS: Induction of acute lung injury by 0.08 mL/kg oleic acid intravenously. Hypoxic pulmonary vasoconstriction inhibition by Escherichia coli endotoxin microdose (15 microg/kg) pretreatment or by metabolic alkalosis (pH 7.60). MEASUREMENTS AND MAIN RESULTS: Pulmonary arterial and venous resistances were determined by flow-pressure curves and by capillary pressure estimation. Regional lung water and pulmonary blood flow were assessed by positron emission tomography. Oleic acid alone increased the arterial and venous resistances, redistributed blood flow away from edematous areas, and decreased the Pao2 from 507 +/- 16 to 373 +/- 60 torr. on Fio2 1.0 and positive end-expiratory pressure 5 cm H2O. Endotoxin pretreatment inhibited the increase in arterial resistance, suppressed the redistribution, and decreased the Pao2 to 105 +/- 22 torr. Alkalosis inhibited the increase in arterial and venous resistances, suppressed the redistribution, and decreased the Pao2 to 63 +/- 12 torr. Reversal of the alkalosis increased the arterial and venous resistances, restored the perfusion redistribution, and improved the Pao2 to 372 +/- 63 torr. Changes in blood gases conformed to predictions of a computer lung model in which hypoxic pulmonary vasoconstriction was suppressed by endotoxin and alkalosis. CONCLUSIONS: We conclude that in oleic acid-induced lung injury, a) pulmonary hypertension results from increases in both arterial and venous resistances; b) the increase in arterial resistance is the primary mechanism responsible for the perfusion redistribution and the gas exchange protection; and c) the increase in arterial resistance is most consistent with hypoxic pulmonary vasoconstriction.

Animals↗

PubMed1989

Regulation of lung surfactant secretion by intracellular pH.

We investigated secretion of lung surfactant phosphatidylcholine (PC) using isolated perfused rat lung preparation after labeling the lung lipids in vitro with [methyl-3H]choline. The perfusion medium was Krebs-Ringer bicarbonate buffer (pH 7.4) containing 10 mM glucose and 3% fatty acid-poor bovine serum albumin. After ventilation of lungs with air containing 5% CO2 (control) for 1 h, 0.91% +/- 0.04 (mean +/- SE, n = 6) of total lung lipid radioactivity (greater than 95% in PC) was recovered in the cell-free lavage fluid. The secretion of PC was increased with terbutaline (50 microM), 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP, 100 microM), phorbol L2-myristate 13-acetate (30 ng/ml), and ATP (1 mM), in each case by approximately 150%. Secretion of PC was also increased by 160% if the lungs were ventilated with air containing 0% CO2. The low CO2-mediated PC secretion was time and concentration dependent. The dose-response curve for 0-10% CO2 was S-shaped. The low CO2-induced increase in PC secretion could be largely reversed with diffusible weak acids (25 mM, acetate or butyrate) in the perfusion medium. An increase (70%) in secretion was also induced with 10 mM NH4Cl, suggesting a role for intracellular alkalosis. These observations suggest that intracellular alkalosis stimulates lung surfactant secretion. Alkalosis-stimulated secretion of PC was additive with that with terbutaline (5 X 10(-7) to 5 X 10(-4) M) or 10(-4) M 8-BrcAMP, suggesting that alkalosis effect was not mediated through the beta-adrenergic pathway of surfactant secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMed1990

Maturation of HCO3- transport in rabbit collecting duct.

Newborn rabbits maintain a state of hypochloremic metabolic alkalosis with plasma HCO3- concentrations generally exceeding 27 mM. The large amounts of potential net base in mother's milk probably contribute to the generation of this alkalosis. We surmised that immature handling of H+ or HCO3- by the neonatal collecting duct helps maintain this alkalosis. Net HCO3- transport was measured in perfused collecting ducts taken from maturing rabbits, in solutions simulating adult rabbit plasma ultrafiltrate and then in presence of Cl(-)-free bathing solution. Cortical collecting ducts (CCD) from newborn and 4-wk-old rabbits failed to secrete HCO3- under baseline conditions and could not be stimulated to secrete HCO3- in Cl(-)-free bath. Neonatal segments perfused at very slow flow rates showed significant HCO3- absorption; inhibition of HCO3- secretion by removal of luminal Cl- revealed a substantial HCO3- absorptive flux. Segments from 6-wk-old and mature animals secreted net HCO3- and generally showed more than a fivefold increase in HCO3- secretion after Cl- removal from the bath. Outer medullary collecting ducts (OMCD) from newborn rabbits absorbed HCO3- at rates approaching that of mature segments. We conclude that relatively high rates of HCO3- absorption in OMCD and lack of HCO3- secretion in CCD may contribute to the metabolic alkalosis of the neonatal rabbit.

Absorption↗

PubMed1984

Metabolic and respiratory hydrogen ion effects on hypoxic pulmonary vasoconstriction.

Hypoxic pulmonary vasoconstriction (HPV) was studied in the ventilated-perfused rat lung in vitro. Respiratory acidosis and alkalosis were obtained by ventilating with 2, 7, or 10% CO2 (21% O2-balance N2). Metabolic acidosis and alkalosis were produced by the addition of 0.9 N NaHCO3 or 1 N lactic acid to the perfusate at constant PCO2. At each pH the pressor responses to 2 and 4% O2 were compared with the maximum pressor response (R%max) obtained with zero O2 and 5% CO2 at a normal pH (approximately 7.35). HPV was maximal when the [H+] was between 38 and 50 nM and was attenuated by changes of pH in either direction. Both respiratory and metabolic pH changes had similar effects. The combined linear regression equations were as follows: with 2% O2 the response to acidosis was R%max = 101.37 - 0.52 [H+] and to alkalosis was R%max = 2.03 [H+] - 3.85; with 4% O2 the response to acidosis was R%max = 56.88 - 0.3 [H+] and to alkalosis was R%max = 1.16 [H+] - 4.95. These effects were not due to changes of ionized calcium.

Animals↗

PubMedDate not supplied

Acid-base state in patients after cardiac transplantation.

Patients with advanced heart failure commonly develop simple or mixed acid-base disturbances. The altered acid-base homeostasis can occur as a consequence of the heart failure itself, the therapeutic interventions, or associated conditions. The present study examined acid-base disorders in patients with heart failure who received successful heart transplantation. The information collected should provide light on the determinants of acid-base disorders in this patient population. Seventy status 2 UNOS (United Network Organ Sharing) patients listed for heart transplantation were enrolled in this study. All patients received loop diuretics, spironolactone, ACE inhibitors, carvedilol and digitalis as needed. Patients were studied again at discharge after transplantation, under cyclosporine, azathioprine, steroids, loop diuretics and ACE inhibitors. After heart transplantation, a significant increase of ejection fraction from 19.7 +/- 0.63 to 53.6 +/- 0.9% (p < 0.0001) occurred along with a concomitant reduction of central venous pressure (p < 0.0001) from 12.6 +/- 0.20 to 6.9 +/- 0.21 mm Hg. Before heart transplantation there was high-normal pH (7.43 +/- 0.009), slight loss of hydrogen ions (35.4 +/- 0.4 nmol/l), slightly reduced pCO(2 )(37.6 +/- 1.1 mm Hg). After heart transplantation a stability of blood pH and hydrogen ion concentrations was found but bicarbonate increased significantly (p < 0.02) from 24.2 +/- 0.61 to 26.2 +/- 0.51 mmol/l and pCO(2) from 37.6 +/- 1.1 to 39.3 +/- 0.7 mm Hg (p < 0.05). Plasma renin activity averaged 3.80 +/- 0.6 pg/ml before heart transplantation and 2.82 +/- 0.4 pg/ml after (p < 0.01). Aldosterone concentration averaged 380 +/-15 pg/ml before heart transplantation and 280 +/- 10 pg/ml after (p < 0.01). These data suggest that in patients before heart transplantation there is a mixed acid-base imbalance that includes respiratory alkalosis and metabolic alkalosis. After transplantation the recovery of the abnormal circulatory status erased the initial respiratory alkalosis but metabolic alkalosis persisted and accounted for a further rise in plasma bicarbonate.

Acid-Base Imbalance↗

PubMed2005

Functional and molecular adaptation of Cl/HCO3- exchanger to chronic alkaline media in renal cells.

The Cl(-)/HCO3- exchanger (AE) is one of the mechanisms that cells have developed to adjust pH Despite its importance, the role of AE isoforms in controlling steady-state pH during alkalosis has not been widely investigated. In the present study, we have evaluated whether conditions simulating acute and chronic metabolic alkalosis affected the transport activity and protein levels of Cl-/HCO3- exchangers in a rat cortical collecting duct cell line (RCCD1). pH(i) was monitored using the fluorescent dye BCECF in monolayers grown on permeable supports. Anion exchanger function was assessed by the response of pH(i) to acute chloride removal. RT-PCR and immunoblot assays were also performed. Our results showed that RCCD1 cells express two members of the anion exchanger gene family: AE2 and AE4. Functional studies demonstrated that while in acute alkalosis pH(i) became alkaline and was not regulated, after 48 h adaptation; steady-state pH(i) reached a value similar to the physiological one. Chronic treated cells also resulted in a 3-fold rise in Cl(-)/HCO3- exchange activity together with a 2.2-fold increase in AE2, but not AE4, protein abundance. We conclude that RCCD1 cells can adapt to chronic extracellular alkalosis reestablishing its steady-state pH(i) and that AE2 would play a key role in cell homeostasis.

Adaptation, Physiological↗

PubMed2003

Crosstalk between voltage-independent Ca2+ channels and L-type Ca2+ channels in A7r5 vascular smooth muscle cells at elevated intracellular pH: evidence for functional coupling between L-type Ca2+ channels and a 2-APB-sensitive cation channel.

This study was designed to investigate the role of voltage-independent and voltage-dependent Ca2+ channels in the Ca2+ signaling associated with intracellular alkalinization in A7r5 vascular smooth muscle cells. Extracellular administration of ammonium chloride (20 mmol/L) resulted in elevation of intracellular pH and activation of a sustained Ca2+ entry that was inhibited by 2-amino-ethoxydiphenyl borate (2-APB, 200 micromol/L) but not by verapamil (10 micro;mol/L). Alkalosis-induced Ca2+ entry was mediated by a voltage-independent cation conductance that allowed permeation of Ca2+ (PCa/PNa approximately 6), and was associated with inhibition of L-type Ca2+ currents. Alkalosis-induced inhibition of L-type Ca2+ currents was dependent on the presence of extracellular Ca2+ and was prevented by expression of a dominant-negative mutant of calmodulin. In the absence of extracellular Ca2+, with Ba2+ or Na+ as charge carrier, intracellular alkalosis failed to inhibit but potentiated L-type Ca2+ channel currents. Inhibition of Ca2+ currents through voltage-independent cation channels by 2-APB prevented alkalosis-induced inhibition of L-type Ca2+ currents. Similarly, 2-APB prevented vasopressin-induced activation of nonselective cation channels and inhibition of L-type Ca2+ currents. We suggest the existence of a pH-controlled Ca2+ entry pathway that governs the activity of smooth muscle L-type Ca2+ channels due to control of Ca2+/calmodulin-dependent negative feedback regulation. This Ca2+ entry pathway exhibits striking similarity with the pathway activated by stimulation of phospholipase-C-coupled receptors, and may involve a similar type of cation channel. We demonstrate for the first time the tight functional coupling between these voltage-independent Ca2+ channels and classical voltage-gated L-type Ca2+ channels.

Ammonium Chloride↗

PubMed1976

Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2.

Hypobaric hypoxia causes hypocapina and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O2 tension of 55 torr for 5 days with 3.77% CO2 added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2 tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2 tension being 39 torr. By contrast, three men at high altitude without CO2 supplementation (PB=455 torr; alveolar PO2=56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial PO2 (48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2 but in the group without CO2 catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2 added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.

Adult↗

PubMed2006

N-methyl-isobutyl-amiloride ameliorates brain injury when commenced before hypoxia ischemia in neonatal mice.

Underphysiologic conditions, brain intracellular pH (pH(i)) is maintained at 7.03. Rebound brain intracellular alkalosis has been observed in experimental models and adult stroke after hypoxia/ischemia (HI). In term infants with neonatal encephalopathy (NE), an association exists between the magnitude of brain alkalosis and neurodevelopmental outcome, and there is increasing evidence to suggest that alkalosis may be deleterious to cell survival. Activation of the Na(+)/H(+) exchanger (NHE) is thought to be responsible for the rapid normalization of pH(i) and rebound alkalosis after reperfusion. We hypothesized that N-methyl-isobutyl-amiloride (MIA), an inhibitor of the NHE, would reduce brain injury in a model of neonatal HI. Seven-day-old mice underwent left carotid artery occlusion followed by exposure to 8% oxygen for 30 min (moderate insult) or 1 h (severe insult). Animals received MIA or saline 8 hourly starting 30 min before HI. Outcome was determined at 48 h by measuring viable tissue in the injured hemisphere (severe insult) or injury score and TUNEL staining (moderate insult). After the severe insult, MIA had a significant neuroprotective effect increasing forebrain tissue survival from 44% to 67%. After the moderate insult, damage was localized to the hippocampus where treatment resulted in a significant reduction in injury score and in TUNEL-positive cells. MIA was also shown to have a significant overall neuroprotective effect based on injury score after the moderate insult. Amiloride analogues are neuroprotective when commenced before HI in a mouse model.

Amiloride↗

PubMed1995

Effects of extreme pH on the physiology of the Australian 'yabby' Cherax destructor: acute and chronic changes in haemolymph carbon dioxide, acid-base and ionic status

Freshwater habitats throughout the world are becoming increasingly threatened by the likelihood of acidification, but little consideration has been given to the importance of severe alkalization. Acute and chronic fluctuations in haemolymph acidbase status (PCO2, CCO2 and pH), [Na+] and [Ca2+] were monitored for up to 504 h (21 days) in the Australian freshwater crayfish Cherax destructor exposed to low- and high-pH water. The importance of carapace [Ca2+] during acid exposure was assessed. Crayfish were exposed to pH 7.1, pH 4.5 and pH 8.0 water containing calcium at 500 µmol l-1 while the effect of a lower calcium concentration (50 µmol l-1) was assessed in pH 4.5 water. Cherax in acid water containing 50 µmol l-1 Ca2+ exhibited a significant decrease in CO2 content after 2 h (mean decrease 1.13 mmol l-1, venous; 1.57 mmol l-1, arterial) and large ranges in PCO2 throughout the treatment (2.47.3 mmHg). The overall acidbase response was a metabolic acidosis compensated by a respiratory alkalosis. The haemolymph Na+ concentration in both control (pH 7.1, 50 µmol l-1) and acid-exposed animals in lower-Ca2+ water was up to 50 % reduced compared with that in animals in pH 7.1, 500 µmol l-1 Ca2+ water. Ion regulatory mechanisms, causing a subsequent increase in haemolymph [Na+] after 288 h, were implicated as an important component in acidbase homeostasis. Crayfish in acid, low-Ca2+ water also exhibited a 3.2 mmol l-1 increase in haemolymph [Ca2+] and showed a haemolymph alkalosis compared with animals in acid water with higher [Ca2+]. At higher water [Ca2+] in pH 4.5 water (500 µmol l-1 Ca2+), the haemolymph pH of Cherax was only 0.1 unit lower than that of animals in 50 µmol l-1 Ca2+ acid water after 96 h, and both CaCO2 and CvCO2 were unchanged compared with the initial condition. As with low-Ca2+ acid-exposure, the potential haemolymph acidosis appeared largely to be compensated by respiratory alkalosis. There was a transient 31 % reduction in haemolymph [Na+], although osmolality was unchanged (control 411±7.29 mosmol kg-1). Acidbase equilibrium recovered rapidly, probably in association with changes in ion flux and the re-establishment of normal haemolymph Na+ concentration. Alkaline-exposed Cherax destructor exhibited a mixed respiratory alkalosis and metabolic acidosis. Whereas haemolymph [Ca2+] increased by 1.8 mmol l-1 after only 1 h, haemolymph Na+ levels increased by 36 % after 2 h, possibly as part of a net H+ loss from the haemolymph. Increased HCO3-/Cl- exchange could contribute to the 4.3 mmol l-1 decrease in haemolymph CO2 level after 0.5 h of alkaline exposure. The responses of Cherax to extreme pH are different from those of the European and North American crayfish species studied to date.

Journal Article↗

PubMed1980

Effect of pH on lipolysis, cAMP and cAMP-dependent protein kinase activity in isolated rat fat cells.

The effect of acidosis and alkalosis on lipolysis, cAMP production and cAMP-dependent protein kinase activity in isolated rat fat cells incubated in the presence of norepinephrine and norepinephrine plus theophylline has been investigated. The pH of the incubation medium was adjusted to 6.8, 7.4 and 7.8 respectively. Acidosis inhibited both norepinephrine- and norepinephrine plus theophylline-induced release of glycerol whereas alkalosis led to slight stimulation. Norepinephrine produced an increase in cAMP and cAMP-dependent protein kinase activity. However, comparison of both parameters in acidosis and alkalosis with those at pH 7.4 indicates that they were higher at pH 7.8 and lower at pH 6.8. Addition of theophylline in combination with norepinephrine increases cAMP production within 5 min, under acidosis to values similar to those obtained at pH 7.4 with norepinephrine. The same effect on protein kinase activity was obtained. In spite of this increment in cAMP and protein kinase activity produced by addition of norepinephrine plus theophylline, lipolysis remains inhibited by acidosis. Addition of theophylline at pH 7.4 and 7.8 induced a much higher cAMP production and cAMP-dependent protein kinase activity although at pH 7.8 there was a statistically significant increase in protein kinase activity at 10 min it did not induce a significant increase in lipolysis. This is discussed and possible mechanisms are suggested to explain the effect of acidosis and alkalosis on the lipolysis induced by norepinephrine in rat fat cells.

Adipose Tissue↗

PubMed1977

[Changes in the acid-base condition and gas composition of the blood in meningoencephalitis of meningococcal etiology].

A study of the acid-base state in meningococcous meningoencephalitis demonstrates that there are different metabolic changes: metabolic acidosis, metabolic alkolosis, respiratory alkalosis and metabolic and respiratory alkalosis. These studies also detected a significant correlation between the character of these changes and syndromes of brain lesions. Deep lesions are characterized by metabolic acidosis, basal-stem lesions by respiratory alkalosis, multiple lesions--by metabolic alkalosis. These data give ground to speak of the significance of brain pathology in the pathogenesis of general metabolic disturbances in meningococcus infections.

Acid-Base Imbalance↗

PubMed2004

[Analysis and adjustment of acid-base disturbances according to the Stewart-Fencl principle].

In 1983, P. J. Stewart proposed a new approach for evaluation of acid-base balance of body fluids. He defined three independent variables responsible for hydrogen ion concentration in body fluids: 1. the partial pressure of carbon dioxide (pCO2); 2. strong ion difference, SID, i.e. the difference between the sums of all the strong (fully dissociated, chemically nonreacting) cations and sums of the strong anions; 3. the total concentration of all the non-volatile weak acids (mainly albumin) designated as [Atot]. On the basis of this theory, V. Fencl invented a new classification of clinical acid-base disturbances. Respiratory acidosis and alkalosis result from abnormalities of pCO2. The classifications of the respiratory disturbances of ABR is identical as in the conventional viewing which is based on the dissociation equation of carbonic acid. Metabolic acidoses or alkaloses result from derangements of the SID and/or [Atot]. The change of SID value is a consequence of either dehydration (alkalosis) or hyperhydration (acidosis). Other mechanisms of SID deviation are either changes of serum chloride concentration (an increase causes acidosis, a decrease causes alkalosis) or an increase of concentrations of substances not routinely measured (ketones, lactate, exogenous acids). [Atot] value is determined mainly by the serum albumin concentration (alkalosis in hypoalbuminemia, acidosis in hyperproteinemia). The Stewart-Fencl approach to acid-base balance enables to understand and predict what happens to hydrogen ions in body fluids and to control the pH abnormalities quantitatively.

Acid-Base Equilibrium↗

PubMed1975

[Effects of acid-base changes upon the chronotropic response to norepinephrine (author's transl)].

The effect of changes in pH produced by changing NaHCO2 at constant pCO2 and by changing pCO2 at constant NaHCO2 concentration was studied in the spontaneous beating rat atrium. Alkalosis produced either by changes in pCO2 or in NaHCO2 concentration increased basal heart rate shifting dose-response curves to norepinephrine upwards. When these dose-response curves were analysed for a horizontal shift, it was found that the necessary dose to produce a given effect was lesser in alkalosis than in acidosis. This shift was significant at the ED10 and at ED30 when the pCO2 was lowered and at ED30, ED50 and ED70 when the NaHCO2 concentration was increased. Beta-adrenergic blockade did not prevent the rate increasing effect of alkalosis. Our results suggest that there is a sensitizing effect to norepinephrine in alkalosis superimposed to a direct effect of pH upon heart rate.

Acid-Base Equilibrium↗

PubMed1983

Effects of disturbances of acid-base equilibrium on the activity of the rumen.

The effect on ruminal motility of NH4- or Na-acetate and Na- or K-lactate of various pH and doses infused into the jugular vein (i.v.) or carotid artery (i.a.) was studied in sheep with ruminal fistula I.v. infusion of NH4-acetate whenever it was accompanied by a considerable increase of the blood NH4 level potently inhibited the amplitude and frequency of ruminal contractions. I. a. administration produced more rapid and more apparent responses and a slightly elevated venous ammonia concentration than did the i.v. infusion. Thus the augmented blood ammonia level not only affected the smooth muscles and peripheral nerve endings but also inhibited the vegetative centres of the central nervous system. Infusion of Na-acetate and Na- or K-lactate solutions induced compensated acidosis or alkalosis which reduced the amplitude of ruminal contractions and produced respiratory disturbances. The latter were more apparent in alkalosis. In uncompensated acidosis or alkalosis, ruminal motility was permanently inhibited or abolished. The results appear to show that in not properly fed ruminants the frequently observed and long lasting compensated acidosis or alkalosis might influence the activity of the vegetative centres thus further metabolic disturbances and impaired gastrointestinal activity might follow the shifts in acid-base equilibrium.

Acid-Base Equilibrium↗

PubMedDate not supplied

[Disorders of acid-base equilibrium in the cerebrospinal fluid after intracranial operations].

The authors collected 27 patients after intracranial operations in whom the cerebrospinal fluid was investigated at least 3 times during 10 days. The patients were divided into 2 groups--a group of 16 patients with favourable outcome, and a group of 11 patients who died. On the basis of arithmetical means of pCO2 and HCO3 values hypothetical curves of the course of acid-base equilibrium in the blood and cerebrospinal fluid were plotted in both groups during 10 days. In the initial period metabolic acidosis was found in the cerebrospinal fluid and respiratory alkalosis in the blood in both groups. After several days metabolic alkalosis developed in the group of patients with favourable outcome while the metabolic acidosis in the cerebrospinal fluid was balanced. In the group with unfavourable outcome metabolic alkalosis in the blood was less evident and metabolic acidosis in the cerebrospinal fluid was increased. The authors think that metabolic alkalosis in the blood has a compensatory effect on metabolic acidosis in the cerebrospinal fluid and brain.

Acid-Base Equilibrium↗

PubMed1994

[The mechanism and clinical significance of decreased anion gap in patients with COPD and acid-base imbalance].

The blood-gas and electrolytes of 427 blood samples from patients with COPD and acid-base imbalance were analysed. The results showed that 14 types of acid-base imbalance were present in patients with COPD and the anion gap decreased in 8 types of acid-base imbalance, especially in respiratory acidosis, metabolic alkalosis and coexistence of both. The anion gap in respiratory acidosis and metabolic alkalosis were 0.8 +/- 6.6mmol/L and 2.1 +/- 7.3mmol/L, respectively. The anion gap in respiratory acidosis with metabolic alkalosis was negative. In all patients the HCO3- increased, and the total anion and total cation diminished. The anion gap decreased owing to the diminution of unmeasured anion. Clinically, the criterion for judging metabolic acidosis with increased anion gap is a value of anion gap over 16 mmol/L. But in case respiratory acidosis (or metabolic alkalosis) and metabolic acidosis coexist in a patient, the anion gap for judging metabolic acidosis should be decreased appropriately.

Acid-Base Equilibrium↗

PubMed1993

[Physiology and clinical aspects of the extracellular bicarbonate pool: plea for cognizant use of HCO3-].

OBJECTIVE: Derived from literature data the function of bicarbonate (HCO3-) is described together with its extracellular pool, the regulating organs, and the clinical variations. DATA SOURCES AND SELECTION CRITERIA: The medical German and English literature was reviewed. No special literature retrieval was performed. Results from measurements at the author's laboratory were used. RESULTS: HCO3- may be described as the most potential nonrespiratory buffer base. For a 65 kg patient, the extracellular HCO3- pool amounts to approximately 350 mmol with a maximum tolerance limit of +/- 200 mmol. An influx of H+ ions (acidosis) and/or a reduction in the pCO2 (hyperventilation) will reduce this pool, whereas alkalosis and hypoventilation will enlarge it. The lungs (in close cooperation with the erythrocytes), liver and kidneys all contribute to the regulation of this HCO3- pool. The paramount organ for this regulation seems to be the liver, since it is able, even within a period of only a few hours, to eliminate much larger amounts of H+ ions (and correspondingly release HCO3-) than the kidneys are able to eliminate even under extreme conditions. It is primarily the liver which regulates the size of the HCO3- pool through the metabolism of the so-called metabolizable anions (bases) such as acetate, lactate, malate and citrate. The metabolism of these anions in the form of acetic, lactic, malic or citric acid requires (per mol) 1 mol H+ (acetate, lactate), 2 mol H+ (malate) or even 3 mol H+ (citrate), with the corresponding release of HCO3-. Iatrogenic alterations in the HCO3- pool occur more frequently than previously assumed. Infusion solutions may lead to a dilution acidosis (dilution of HCO3-), an infusion acidosis (addition of H+) or an infusion alkalosis (administration of metabolizable anions). CONCLUSION: An improvement in the declaration accompanying infusion solutions is recommended according to their actual pH-dependent composition. In particular, the concepts of base excess (BE, mmol/l) and BE pot. (mmol/l) should be introduced, in order to give an indication of potential alterations in the HCO3- pool after infusion and metabolism. This also applies to blood derivatives, where transfusion acidosis as well as alkalosis may occur, and in hemodialysis and peritoneal dialysis where the occurrence of acidosis and alkalosis during therapy need to be reckoned with.

Acid-Base Imbalance↗