ACID-BASE LANGUAGE VERSUS ACID-BASE MEASUREMENTS

PEDIATRICS ◽  
1969 ◽  
Vol 43 (5) ◽  
pp. 830-832
Author(s):  
Giles F. Filley

The PAPERS of Kildeberg and Engel and of Nelson and Riegel continue what has been called, inaccurately, "The Great Transatlantic Acid-Base Debate" betsveen two schools of acid-base physiology. Historically at least, these can be called the Continental and Anglo-American Schools and their current dispute a war of words. We will sketch their beginnings, describe some of their differences, and indicate the importance of the distinction between fundamental and derived measurement. The Continental School was probably founded by Hasselbalch, who in 1916 began the apparently never-ending search for a chemical index of a "metabolic component," i.e., a number indicating the quantity of non-volatile acid added to or lost from the body-"corrected" for respiratory effects. Hasselbalch index was typical of the genre because it required exposing a blood specimen in vitro to known CO2 gas mixtures and was called a "reduced hydrogen ion concentration." His successors have tended to work meticulously in chemical laboratories, to give special names to defined magnitudes, and to incorporate these into logical formulations. One example was that of Singer and Hastings, which was based on a thoroughgoing study of blood as a physicochemical system at various states of equilibrium outside the body. Another recent and carefully developed one is that of Siggaard-Andersen. Despite this and other authors warnings, this school formulations are subject to abuse perhaps especially by those who assume that an "Astrup determination" is a substitute for clinical judgement. The other school is less systematic, its members being more often physiologists or physicians than physical chemists.

1982 ◽  
Vol 100 (1) ◽  
pp. 23-40 ◽  
Author(s):  
R G O'Regan ◽  
S Majcherczyk

Adjustments of respiration and circulation in response to alterations in the levels of oxygen, carbon dioxide and hydrogen ions in the body fluids are mediated by two distinct chemoreceptive elements, situated peripherally and centrally. The peripheral arterial chemoreceptors, located in the carotid and aortic bodies, are supplied with sensory fibres coursing in the sinus and aortic nerves, and also receive sympathetic and parasympathetic motor innervations. The carotid receptors, and some aortic receptors, are essential for the immediate ventilatory and arterial pressure increases during acute hypoxic hypoxaemia, and also make an important contribution to respiratory compensation for acute disturbances of acid-base balance. The vascular effects of peripheral chemoreceptor stimulation include coronary vasodilation and vasoconstriction in skeletal muscle and the splanchnic area. The bradycardia and peripheral vasoconstriction during carotid chemoreceptor stimulation can be lessened or reversed by effects arising from a concurrent hyperpnoea. Central chemoreceptive elements respond to changes in the hydrogen ion concentration in the interstitial fluid in the brain, and are chiefly responsible for ventilatory and circulatory adjustments during hypercapnia and chronic disturbances of acid-base balance. The proposal that the neurones responsible for central chemoreception are located superficially in the ventrolateral portion of the medulla oblongata is not universally accepted, mainly because of a lack of convincing morphological and electrophysiological evidence. Central chemosensitive structures can modify peripheral chemoreceptor responses by altering discharges in parasympathetic and sympathetic nerves supplying these receptors, and such modifications could be a factor contributing to ventilatory unresponsiveness in mild hypoxia. Conversely, peripheral chemoreceptor drive can modulate central chemosensitivity during hypercapnia.


1986 ◽  
Vol 110 (2) ◽  
pp. 293-301 ◽  
Author(s):  
K. J. Radke ◽  
R. E. Taylor ◽  
E. G. Schneider

ABSTRACT The direct effects of changes in extracellular hydrogen ion (H+) concentration on aldosterone secretion under basal, angiotensin II- and potassium-stimulated conditions were studied in isolated, perfused canine adrenal glands. Changes in extracellular H+ concentration were induced by altering either the partial pressure of CO2 (pCO2) or the HCO3− concentration of the perfusate. Acid-base disturbances had a more pronounced effect on aldosterone secretion under stimulated than under basal conditions. Increasing H+ concentration enhanced angiotensin II- and potassium-stimulated aldosterone secretion, whereas decreasing H+ concentration markedly inhibited the secretory response to these stimuli. Because changes in H+ concentration, whether produced by varying extracellular pCO2 or extracellular HCO3− concentration, had similar effects on angiotensin II-stimulated aldosterone secretion, the data suggest that H+ concentration per se is the important determinant of the aldosterone secretory rate. Interestingly, during the immediate recovery period from pCO2-induced alkalosis under both angiotensin II- and potassium-stimulated conditions, aldosterone secretion always returned to a value significantly higher than that obtained just before alkalosis. The results of this study demonstrate that changes in extracellular H+ concentration influence the rate of aldosterone secretion, possibly via changes in intracellular pH, by a direct action on the canine adrenal gland. Therefore, when evaluating the control of aldosterone secretion, the acid-base status of the whole animal or of in-vitro adrenal tissue must be considered. J. Endocr. (1986) 110, 293–301


Since changes of hydrogen ion concentration affect reactions catalyzed by the enzymes of the body in vitro, they may be expected to do so in vivo. But as it is impossible to change the reaction of the tissues without altering the concentration of other ions than hydrogen, caution is required in interpreting the results. In the experiments here reported the cH of our tissues was increased by breathing carbon dioxide and drinking ammonium chloride solution, diminished by over-breathing and sodium bicarbonate ingestion, as described by us in a former paper (1). If the same results are produced by two such different methods of increasing or diminishing the cH, they probably spring from this change as common cause; if not, they are probably due to other causes. Methods . Blood sugars were estimated by Bang’s (2) original method. The relation between rotatory and reducing power of the blood sugar before and after hydrolysis was determined for us by Smith and Winter by their method (3). Acetone, aceto-acetic acid and β-oxybutyric acid were determined by Lublin’s (4) method. This proved quite satisfactory for acetone and acetoacetic acid, but it was found that normal urines on heating with potassium bichromate and sulphuric acid gave a small yield of bodies reducing iodine in alkaline solution. However, if (as is probable) the excretion of these per hour remained fairly constant, the correction to be made for their presence was small. Benedict’s (5) solution was used as a qualitative test for sugar in urine. Respiratory metabolism was determined by the method of Douglas (6) after at least half-an-hour’s moderate rest, and 10 minutes’ complete rest in a deck chair, during the last five of which the subject breathed through valves. Fasting metabolisms measured in this way on two days were 1⋅54 and 1⋅57 calories per minute, the corresponding basal values being 1⋅43 and 1⋅47, or 7 per cent. lower. The calorie values of the oxygen are calculated from Carpenter’s (7) tables, neglecting protein metabolism, and the error due to changing CO 2 capacity of the body.


Author(s):  
Aron Chakera ◽  
William G. Herrington ◽  
Christopher A. O’Callaghan

Normal metabolism results in a net acid production of approximately 1 mmol/kg day−1. Physiological pH is regulated by excretion of this acid load (as carbon dioxide) by the kidneys and the lungs. A series of buffers in the body reduces the effects of metabolic acids on body and urine pH. For acid–base disorders to occur, there must be excessive intake (or loss) of acid (or base) or, alternatively, an inability to excrete acid. For these changes to result in a substantially abnormal pH, the various buffer systems must been overwhelmed. The pH scale is logarithmic, so relatively small changes in pH signify large differences in hydrogen ion concentration. Most minor perturbations in acid–base balance are asymptomatic, as small changes in acid or base levels are rapidly controlled through consumption of buffers or through changes in respiratory rate. Alterations in renal acid excretion take some time to occur. Only when these compensatory mechanisms are overwhelmed do symptoms related to changes in pH develop. This chapter reviews the causes and consequences of acid–base disorders.


2001 ◽  
Vol 281 (2) ◽  
pp. G371-G374 ◽  
Author(s):  
Linzi A. Thomas ◽  
Martin J. Veysey ◽  
Gerard M. Murphy ◽  
R. Hermon Dowling

Prolonged large bowel transit time and an associated increase in the proportion of deoxycholic acid (DCA) in serum and bile have been implicated in the development of cholesterol-rich gallstones and colon cancer. Prolongation of intestinal transit also increases intracolonic pH that, we hypothesized, should favor the solubilization and absorption of newly formed DCA within the colon. To test this hypothesis, we performed in vitro studies on homogenized cecal aspirates (obtained at colonoscopy) that were incubated anaerobically with [14C]cholic acid for 16 h after which the pH was adjusted to between 4.0 and 7.0 in 0.5-pH unit steps. The resultant reaction mixtures were centrifuged to separate the supernatant from the precipitate, and the specific activity of [14C]DCA was quantitated in both phases. As the pH in the aspirates was manipulated from 4.0 to 7.0, the proportion of newly formed, labeled DCA increased in the supernatant and fell in the precipitate, particularly at a hydrogen ion concentration of <100 × 10−7 (equivalent to pH 5.0–7.0). These results show that the solubility of DCA in colonic contents increases with increasing pH. If solubility is rate limiting, this should lead to increased absorption that, in turn, would explain why the proportion of DCA in serum and bile increases with the prolongation of large bowel transit time.


1963 ◽  
Vol 204 (6) ◽  
pp. 1048-1054 ◽  
Author(s):  
Ronald B. Miller ◽  
Ian Tyson ◽  
Arnold S. Relman

Intracellular pH of isolated rat diaphragm was measured with both a C14-DMO method and a tissue CO2 technique. The values for intracellular pH by each method, although slightly different, changed in parallel under most experimental conditions. Acute, severe potassium depletion in vitro had no detectable effect on intracellular pH, nor did prior depletion in vivo followed by incubation in a potassium-free bath. This was true whether or not the potassium-depleted muscle was exposed to normal or elevated extracellular levels of bicarbonate, and was unaffected by the presence of cationic amino acids in the bath. Acute repletion of previously potassium-depleted muscle resulted in a small rise in cell pH, but this was no greater than that produced by loading normal tissues with potassium. It is concluded that under the conditions of these experiments there is no evidence of intracellular acidosis in potassium-depleted skeletal muscle. Rat diaphragm can lose up to half its potassium content in vitro without detectable increase in hydrogen ion concentration.


1918 ◽  
Vol 1 (2) ◽  
pp. 237-254 ◽  
Author(s):  
Jacques Loeb

1. It is shown by volumetric analysis that on the alkaline side from its isoelectric point gelatin combines with cations only, but not with anions; that on the more acid side from its isoelectric point it combines only with anions but not with cations; and that at the isoelectric point, pH = 4.7, it combines with neither anion nor cation. This confirms our statement made in a previous paper that gelatin can exist only as an anion on the alkaline side from its isoelectric point and only as a cation on the more acid side of its isoelectric point, and practically as neither anion nor cation at the isoelectric point. 2. Since at the isoelectric point gelatin (and probably amphoteric colloids generally) must give off any ion with which it was combined, the simplest method of obtaining amphoteric colloids approximately free from ionogenic impurities would seem to consist in bringing them to the hydrogen ion concentration characteristic of their isoelectric point (i.e., at which they migrate neither to the cathode nor anode of an electric field). 3. It is shown by volumetric analysis that when gelatin is in combination with a monovalent ion (Ag, Br, CNS), the curve representing the amount of ion-gelatin formed is approximately parallel to the curve for swelling, osmotic pressure, and viscosity. This fact proves that the influence of ions upon these properties is determined by the chemical or stoichiometrical and not by the "colloidal" condition of gelatin. 4. The sharp drop of these curves at the isoelectric point finds its explanation in an equal drop of the water solubility of pure gelatin, which is proved by the formation of a precipitate. It is not yet possible to state whether this drop of the solubility is merely due to lack of ionization of the gelatin or also to the formation of an insoluble tautomeric or polymeric compound of gelatin at the isoelectric point. 5. On account of this sudden drop slight changes in the hydrogen ion concentration have a considerably greater chemical and physical effect in the region of the isoelectric point than at some distance from this point. This fact may be of biological significance since a number of amphoteric colloids in the body seem to have their isoelectric point inside the range of the normal variation of the hydrogen ion concentration of blood, lymph, or cell sap. 6. Our experiments show that while a slight change in the hydrogen ion concentration increases the water solubility of gelatin near the isoelectric point, no increase in the solubility can be produced by treating gelatin at the isoelectric point with any other kind of monovalent or polyvalent ion; a fact apparently not in harmony with the adsorption theory of colloids, but in harmony with a chemical conception of proteins.


2015 ◽  
Vol 1112 ◽  
pp. 449-452 ◽  
Author(s):  
Deni Noviana ◽  
Sri Estuningsih ◽  
Devi Paramitha ◽  
Mokhammad Fakhrul Ulum ◽  
Hendra Hermawan

A foreign body is any object originating outside the body. It may migrate from its entry site and cause pain, inflammation and infection. This study aims to examine in vitro cytotoxicity and in vivo tissue response at different implantation sites of two iron-based foreign body (FeFB) specimens: pure Fe wire, Cr-coated Fe wire, and SS316L wire as control. In vitro cytotoxicity was assessed towards rat smooth muscle cells with direct method of methyl thiazolyl tetrazolium (MTT) assay. In vivo tissue response was examined using mice animal model until day 14 after surgical implantation in subcutaneous nape area and intramuscular right femoral muscle. Cell viability, surface morphology and Fe ion release were examined. Implant density and tissue response were examined by using radiographic imaging and histology, respectively. Results showed that both FeFB specimens exhibited similar cell viability with SS316L. Iron ion concentration was higher in both FeFB medium compared to that of SS316L and with oxide layer formation on their surface. Radiographic analysis showed that the density of both FeFB implants end-side was increased. Meanwhile, histological tissue response at intramuscular sites for FeFB specimens showed a prominent inflammatory response compared to SS316L. Detailed analysis on cell and tissue-material interactions of the iron-based foreign body specimens is discussed further in this article.


Author(s):  
Kwok M. Ho

Anatomically the kidney consists of the cortex, medulla, and renal pelvis. The kidneys have approximately 2 million nephrons and receive 20% of the resting cardiac output making the kidneys the richest blood flow per gram of tissue in the body. A high blood and plasma flow to the kidneys is essential for the generation of a large amount of glomerular filtrate, up to 125 ml min−1, to regulate the fluid and electrolyte balance of the body. The kidneys also have many other important physiological functions, including excretion of metabolic wastes or toxins, regulation of blood volume and pressure, and also production and metabolism of many hormones. Although plasma creatinine concentration has been frequently used to estimate glomerular filtration rate by the Modification of Diet in Renal Disease (MDRD) equation in stable chronic kidney diseases, the MDRD equation has limitations and does not reflect glomerular filtration rate accurately in healthy individuals or patients with acute kidney injury. An optimal acid–base environment is essential for many body functions, including haemoglobin–oxygen dissociation, transcellular shift of electrolytes, membrane excitability, function of many enzymes, and energy production. Based on the concepts of electrochemical neutrality, law of conservation of mass, and law of mass action, according to Stewart’s approach, hydrogen ion concentration is determined by three independent variables: (1) carbon dioxide tension, (2) total concentrations of weak acids such as albumin and phosphate, and (3) strong ion difference, also known as SID. It is important to understand that the main advantage of Stewart over the bicarbonate-centred approach is in the interpretation of metabolic acidosis.


Sign in / Sign up

Export Citation Format

Share Document