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Query: UMLS:C0847097 (acidity)
15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is generally believed that the reduction in plasma [HCO3] characteristic of chronic hypocapnia results from renal homeostatic mechanisms designed to minimize the alkalemia produced by.the hypocapneic state. To test this hypothesis, we have induced chronic hypocapnia in dogs in which plasma [HCO3] had previously been markedly reduced (from 21 to 15 meq/liter) by the prolonged feeding of HCl. The PaCO2 of chronically acid-fed animals was reduced from 32 to 15 mm Hg by placing the animials in a large environmental chamber containing 9% oxygen. In response to this reduction in PaCO2, mean plasma [HCO3] fell by 8.6 meq/liter, reaching a new steady-state level of 6.4 meq/liter. This decrement in plasma [HCO3] is almost identical to the 8.1 meq/liter decrement previously observed in normal (nonacid-fed) animals in which the same degree of chronic hypocapnia had been induced. Thus, in both normal and HCl-fed animals, the renal response to chronic hypocapnia causes plasma [HCO3] to fall by approximately 0.5 meq/liter for each millimeter of Hg reduction in CO2 tension. By contrast, the response of plasma [H+] in the two groups was markedly different. Instead of the fall in [H+] which is seen during chronic hypocapnia in normal animals, [H+] in HCl-fed animals rose significantly from 53 to 59 neq/liter (pH 7.28-7.23). This seemingly paradoxical response is, of course, an expression of the constraints imposed by the Henderson equation and reflects the fact that the percent fall in [HCO3] in the HCl-fed animals was greater than the percent fall in PaCO2. These findings clearly indicate that in chronic hypocapnia the kidney cannot be regarded as the effector limb in a homeostatic feedback system geared to the defense of systemic acidity.
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PMID:Regulation of acid-base equilibrium in chronic hypocapnia. Evidence that the response of the kidney is not geared to the defense of extracellular (H+). 0 88

Acid-base physiology is concerned with sources, extent, and control of hydrogen ion donation in the body, at the organ-physiological as well as the molecular level of study. With the introduction of Van Slyke's methods for quantitative carbon dioxide measurements in biological fluids, one important source of hydrogen ion donation became identifiable; and these and derived methods have permitted of fairly precise quantitative descriptions of transport and pulmonary elimination of carbon dioxide. However, the inevitable operational concept of non-carbonic (non-volatile) contributions to the titratable acidity of the body fluids has been a cause of considerable methodological and conceptual difficulties; and whereas it is now possible by means of the micro-equilibration technique to make accurate assessments of the concentration of non-volatile titratable acid (base) in blood, the question of the physiological relevance of the concept of 'base excess' remains open. In particular, the concept of non-carbonic acid does not possess a specific relevance with respect to the acid-base physiology of kidney, bone, and gastro-intestinal tract comparable to the 'substrate-specificity of carbon dioxide with respect to the lung. Our studies indicate that a subdivision of the titratable non-carbonic acid of any biological medium in two subcomponents will provide an improvement of specificity, adequate for a system physiological approach at the organ level. Thus, a distinction should be made between (1) processes of hydrogen ion donation, reversible by endogenous metabolic means (quantitated in terms of the component MA = metabolizable non-carbonic acid) and (2) processes of hydrogen ion donation associated with gastro-intestinal, skeletal, and renal transport, storage, and control of non-metabolizable non-carbonic acid (NA). Some implications of this distinction for acid-base physiology and acid-base diagnostics are discussed.
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PMID:Physiological viewpoints on clinical acid-base diagnostics. 1 79

A basic premise in the utilization of the plasma anion gap in the assessment of acid-base disorders is that this parameter remains constant during hyperchloremic metabolic acidosis and metabolic alkalosis. Experimental data under in vitro conditions, however, cast serious doubt on this premise. The purpose of the present study was to characterize the plasma anion gap, estimated as (Na + K) - Cl + HCO3), in two large groups of dogs with graded degrees of chronic, HCl-induced metabolic acidosis or chronic, diuretic-induced metabolic alkalosis. The data indicate that the plasma anion gap decreases significantly in HCl acidosis and increases significantly in metabolic alkalosis; the predicted mean anion gap in animals with a plasma bicarbonate concentration of 10, 21 (normal), and 40 meq/liter approximated 13, 18, and 26 meq/liter, respectively. The observed variation in the plasma anion gap is interpreted as originating mainly from directional changes in the net negative charge of plasma proteins; these changes result from the titration process secondary to the altered plasma acidity and, in the case of metabolic alkalosis, from the additional effect of an increased plasma protein concentration.
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PMID:Changes in the plasma anion gap during chronic metabolic acid-base disturbances. 2 93

An Aspergillus flavus strain isolated from Egyptian soil produced fat in appreciable amounts. General evidence for the operation of the tricarboxylic acid cycle in this organism has been ascertained by the detection of citric, malic and fumaric acids in the metabolized culture solution. Maximum fat yield was attained after seven days of incubation. The lower intial pH value of the media favoured the fat obtained from the felts and raised its acid value. When the felts were sterilized in their acidic metabolism solutions increased the acid values of the fats over those of fats extracted from felts sterilized in distilled water. The felts autoclaved for the longest time produced the highest yields of fat with the highest free acidity. The employment of calcium carbonate in the nutrient solutions raised appreciably the acid values of the fats and suppressed the other metabolic activities.
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PMID:Biosynthesis of fat in surface culture of a local strain of Aspergillus flavus. 4 Mar 64

Total and regional cerebral blood flow (CBF), and cerebrospinal fluid (CSF), and arterial blood acid-base status were measured in 26 chloralose-urethan-anesthetized dogs before and after 30 and 60 min of ventriculocisternal perfusion with artificial CSF equilibrated with 7% CO2 and containing either low (8.7 or 9.1 meq/l), normal (19.6 meq/l), or high (34.7 meq/l) bicarbonate ion concentration ([HCO3-]). An inverse linear relationship was observed between the CSF pH and total CBF. Regional blood flow changes were greater in structures that were closest to the ventricular system. In addition, regional blood flow changes were greater in all tissues studied after 60 min of perfusion than after 30. Perfusion with the control [HCO3-] caused no significant changes in either acid-base status or CBF. We believe that the regional cerebral blood flow changes are the result of changes in the H+ concentration gradient across the cerebral extracellular fluid (ECF) space due to the diffusional exchange of HCO3- between CSF and ECF. It is concluded that cerebral ECF acidity is important in the local regulation of cerebral blood flow.
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PMID:Effect of cerebral extracellular fluid acidity on total and regional cerebral blood flow. 4 28

Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
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PMID:The apparent buffer value of cerebrospinal fluid in acute hypercapnia. 82 71

The effects of parenteral pilocarpine, atropine, and norepinephrine on salt and water transport were studied in jejunum and ileum of anesthetized rats. Pilocarpine increased jejunal transmural PD, reduced absorption of Na, K, HCO3, and H2O, and increased secretion of Cl; in ileum, it caused secretion of Na and H2O, elicited secretion of K, and reduced the absorption of Cl. In both segments, perfusate became more akaline, and there was less of a rise in PCO2. Atropine prevented all changes caused by pilocarpine. Atropine alone increased jejunal absorption of Na and HCO3 and acidity of perfusate, implying that cholinergic nerves influence transport. Norepinephrine augmented jejunal absorption of Na, Cl, and H2O but caused no change in PD. In ileum, norepinephrine increased absorption of Na and Cl, reduced the rise in pH, increased the rise in PCO2 of perfusate, but did not affect net HCO3 movement. With all agents, when Na absorption increased, perfusate became more acidic in jejunum and less alkaline in ileum, evidence of an association between Na and H transport.
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PMID:Intestinal ion transport: effect of norepinephrine, pilocarpine, and atropine. 96 67

The study comprised a series of 16 neonates made up of 5 patients of 33 weeks of gestation, 5 infants of 35 weeks and 6 more of 40 weeks of gestation. Blood pH, PaCO2 and HCO3- were measured together with bicarbonate, ammonium, titrable acidity and hydrogen ions in urine before and after intravenous infusion of sodium bicarbonate. Before infusion of bicarbonate, titrable acidity, ammonium and net acidity in urine were higher in accordance with a greater gestational age. As the administration of bicarbonate elapsed, titrable acidity, ammonium and net acidity dropped with increase in concentration of bicarbonate. A hypothesis is set forth that the differences found in the factors evaluated in urine before administration of bicarbonate depend on the physiologic characteristics set in the newborn by gestational age.
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PMID:[Renal response to intravenous administration of sodium bicarbonate in newborn infants of different gestational ages]. 124 69

The course of intracellular pH (pHi) was followed in superfused (36 degrees C) single glomus (type I) cells of the freshly dissociated adult rat carotid body. The cells had been loaded with the pH-sensitive fluorescent dye 2',7'-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein. The high K(+)-nigericin method was used for calibration. The pHi of the glomus cell at pHo 7.40, without CO2, was 7.23 +/- 0.02 (n = 70); in 5% CO2/25 mM HCO3-, pHi was 7.18 +/- 0.08 (n = 9). The pHi was very sensitive to changes in pHo. Without CO2, delta pHi/delta pHo was 0.85 (pHo 6.20-8.00; 32 cells), while in CO2/HCO3- this ratio was 0.82 irrespective of whether pHo (6.80-7.40; 14 cells) was changed at constant PCO2 or at constant [HCO3-]o. The great pHi sensitivity of the glomus cell to pHo is matched only by that of the human red cell. An active Na+/H+ exchanger (apparent Km = 58 +/- 6 mM) is present in glomus cells: Na+ removal or addition of the amiloride derivative 5-(N,N-hexamethylene)-amiloride induced pHi to fall by as much as 0.9. The membrane of these cells also contains a K+/H+ exchanger. Raising [K+]o from 4.7 to 25, 50, or 140 mM reversibly raised pHi by 0.2, 0.3, and 0.6, respectively. Rb+ had no effect, but in corresponding concentrations of Tl+ alkalinization was much faster than in K+. Reducing [K+]o to 1.5 mM lowered pHi by 0.1. These pHi changes were shown not to be due to changes in membrane voltage, and were even more striking in the absence of Na+. Intrinsic buffering power (amount of strong base required to produce, in the nominal absence of CO2, a small pHi rise) increased from 3 to approximately 21 mM as pHi was lowered, but remained nearly unchanged below pHi 6.60. The fitted expression assumed the presence of one "equivalent" intracellular buffer (pK 6.41, 41 mM). The exceptional pHi sensitivity to pHo suggests that the pHi of the glomus cell is a link in the chemoreceptor's response to external acidity.
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PMID:pH regulation in adult rat carotid body glomus cells. Importance of extracellular pH, sodium, and potassium. 129 52

The deleterious effects of increased gastric pH on calcium absorption from calcium carbonate supplements were observed about 25 years ago. Increasing use of calcium supplements, especially by the elderly, has raised questions about bioavailability from various calcium sources. Decreased gastric acidity is common in the elderly and in patients taking antiulcer medications. A critical review of the available human studies that have investigated the role of gastric acidity in calcium bioavailability suggests that the effects of increased gastric pH are only apparent when poorly soluble calcium salts are taken after an overnight fast. Soluble calcium sources, such as calcium citrate and calcium from milk, are absorbed normally in elderly subjects with atrophic gastritis. Moreover, calcium carbonate, a relatively insoluble calcium salt, is well absorbed in atrophic gastritis patients if administered with a meal. In order to maximize calcium bioavailability, elderly subjects should increase their calcium intakes to at least recommended levels, preferably by increasing milk consumption. When calcium supplements are used to augment dietary calcium sources, a highly soluble source should be of benefit or calcium carbonate may be taken with a meal.
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PMID:Gastric acidity, atrophic gastritis, and calcium absorption. 157 81


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