Disease relevance of Acid-Base Equilibrium

• We evaluated the use of the urinary anion gap (sodium plus potassium minus chloride) in assessing hyperchloremic metabolic acidosis in 38 patients with altered distal urinary acidification and in 8 patients with diarrhea [1].
• In contrast, the anion gap was positive in all patients with altered urinary acidification, who were classified as having classic renal tubular acidosis (23 +/- 4.1 mmol per liter, 11 patients), hyperkalemic distal renal tubular acidosis (30 +/- 4.2, 12 patients), or selective aldosterone deficiency (39 +/- 4.2, 15 patients) [1].
• In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate [2].
• The effect of a meat load on the renal handling of acid-base balance was studied in ten healthy subjects (GFR by inulin clearance = 98.5 +/- 8.14 ml.min-1.1.73 m-2) and in ten patients affected by chronic renal failure (CRF) (GFR = 39.9 +/- 5.3 ml.min-1.1.73 m-2) [3].
• Thus, both the wide prediction interval and volume depletion (as reflected by blood urea nitrogen level) impair the usefulness of the anion gap as a screen for mixed acid-base disorders in patients with diabetic ketoacidosis [4].

Psychiatry related information on Acid-Base Equilibrium

• The acute toxicities of the cellular differentiating agent hexamethylene bisacetamide (HMBA) in humans and animals include CNS toxicity (agitation, somnolence, seizures, hallucinations) and an anion-gap metabolic acidosis [5].
• We report values for CSF and blood lactate and acid-base balance in 8 girls with the Rett syndrome and correlate the findings with respiratory dysfunction [6].
• Clinicians must be aware that differences exist between the ISE technologies and in border-line clinical situations, the direct ISE systems provide a more accurate estimate of plasma sodium, potassium, chloride, anion gap, osmolality and strong ion difference calculations, and should be used for clinical decision-making [7].

High impact information on Acid-Base Equilibrium

• Atp6i-/- mice exhibit a normal acid-base balance in blood and urine [8].
• These data show that NHE3 is the major absorptive Na+/H+ exchanger in kidney and intestine, and that lack of the exchanger impairs acid-base balance and Na+-fluid volume homeostasis [9].
• The increased serum anion gap was caused by hyperproteinemia, lactic acidemia, and hyperphosphatemia, with anionic contributions to the rise in anion gap estimated as protein, 5.5 meq per liter; lactate, 2.5 meq per liter; and phosphate, 2.5 meq per liter [10].
• Iodide and negative anion gap [11].
• Toxic effects of toluene: a new cause of high anion gap metabolic acidosis [12].

Chemical compound and disease context of Acid-Base Equilibrium

• Ethylene glycol intoxication produces a severe metabolic acidosis with an increased anion gap [13].
• Increased renal ammoniagenesis and bicarbonate synthesis from glutamine during chronic metabolic acidosis facilitate the excretion of acids and partially restore normal acid-base balance [14].
• Severe lithium carbonate intoxication should be added to the category of illnesses (multiple myeloma, bromide intoxication) causing a marked reduction in the anion gap [15].
• The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings [16].
• Blood gases and acid-base balance, blood glucose, liver (ATP, glucose, lactate) and brain (ATP, ADP, AMP, CP, glucose, lactate) metabolites were determined in unbled animals and after 35 min hypotension in bled animals [17].

Biological context of Acid-Base Equilibrium

• Effect of acute alterations in acid-base balance on rat renal glutaminase and phosphoenolpyruvate carboxykinase gene expression [18].
• These patients were treated according to a protocol that directed aggressive medical management of fluid balance with electrolyte solutions, plasma, and blood; acid-base balance; coagulation defects with fresh frozen plasma; blood replacement as needed; dietary protein elimination; and orally administered neomycin sulfate [19].
• Hypoxemic resuscitation in newborn piglets: recovery of somatosensory evoked potentials, hypoxanthine, and acid-base balance [20].
• With controlled acid-base balance and temperature, and under 1.0 to 1.2 percent endtidal halothane anesthesia, 5 and microgram/kg of IV fentanyl citrate were given sequentially 1 hour apart and heart rate (HR) followed for 60 minutes [21].
• The values for serum sodium, total CO2, anion gap, potassium, and hematocrit at the end of treatment were similar, whereas total serum calcium was significantly greater following HD [22].

Anatomical context of Acid-Base Equilibrium

• Interestingly, FR167356 treatment did not affect blood acid-base balance; however, FR167356 inhibited renal V-ATPase with a similar potency as for osteoclast V-ATPase inhibition [23].
• In these conditions the reactivity or cerebral blood vessels toward changes in the acid-base balance is altered: the CO2 reactivity is less pronounced, while the effect of increasing the plasma (HCO-3) is more pronounced than in normal cats [24].
• The novel action of aldosterone to inhibit luminal acidification in the MTAL may play a role in enabling the kidney to regulate acid-base balance independently of Na(+) balance and extracellular fluid volume [25].
• Six dogs with normal acid-base equilibrium and eight dogs with chronic metabolic acidosis were infused with valproate directly into their left renal artery in order to obtain arterial concentrations around 3 to 4 mM [26].
• Alterations in acid-base balance significantly affect the amount of the glutaminase that is present in rat kidney, but not in brain or small intestine [27].

Associations of Acid-Base Equilibrium with chemical compounds

• At the time of admission, the mean serum concentration of sodium was 134.8 mmol (meq) per liter, that of chloride was 103.2 mmol per liter, and that of bicarbonate was 11.4 mmol per liter; the mean anion gap was 20.2 mmol per liter [10].
• Mineralocorticoid plays a role in urinary acidification and acid-base balance, but the response of the inner medulla to aldosterone has not been elucidated [28].
• The effects of dopamine and adrenaline infusions on acid-base balance and systemic haemodynamics in severe infection [29].
• Lactate utilization for oxidative purposes and for the resynthesis of glucose is essential for the maintenance of acid-base balance [30].
• Although Dronpa exists in an acid-base equilibrium, only the photoinduced protonated form shows the switching behavior [31].

Gene context of Acid-Base Equilibrium

• However, humans and mice with genetic disruption of Slc26a4 have normal acid-base balance under basal conditions [32].
• Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance [33].
• Cytoplasmic carbonic anhydrase (CA) II is involved in acid-base balance in a wide variety of tissues [34].
• Many catabolic conditions are characterized by disturbances in acid-base balance and concomitant alterations in the insulin-like growth factor (IGF) system [35].
• These results represent the first demonstration of anion exchanger expression in the chick CAM, and they suggest a role for basolateral AE1 in bicarbonate reabsorption that is required in the embryo for maintaining acid-base balance during development [36].

Analytical, diagnostic and therapeutic context of Acid-Base Equilibrium

• Immunohistochemistry on rat lung and kidney sections revealed dense localization of Ig-Hepta in alveolar walls and intercalated cells in the collecting duct, respectively, suggesting a role in the regulation of acid-base balance [37].
• In both subjects, hemodialysis simultaneously removed the excess lithium ion and normalized the anion gap [15].
• The animals were maintained on a ventilator and frequent measurements of acid/base balance, electrolytes, and glucose were made [38].
• BACKGROUND: beta-Adrenergic receptors (beta-ARs) are known to participate in the regulation of glomerular filtration, NaCl reabsorption, acid-base balance, and renin secretion; however, the precise histologic localization of beta-AR at putative signaling sites involved in these processes remains an open issue [39].
• In the fifth patient, CAVH was the sole renal replacement therapy employed; in this critically ill anuric infant, we were best able to evaluate the ability of CAVH to continuously control fluid, electrolyte, and acid-base balance, and allow the administration of adequate parenteral nutrition [40].

References