Chapter 1 The Hydrogen Ion in general Metabolism: A overview (pages 1–19): ok. G. M. M. Alberti and C. Cuthbert
Chapter 2 The options and makes use of of Intracellular pH Measurements (pages 20–35): R. D. Cohen, R. M. Henderson, R. A. Iles, J. P. Monson and J. A. Smith
Chapter three strength Metabolism and mobile pH in general and Pathological stipulations. a brand new glance through 31Phosphorus Nuclear Magnetic Resonance (pages 36–57): George okay. Radda, David G. Gadian and Brian D. Ross
Chapter four Acidosis and Contractility of center Muscle (pages 58–76): P. A. Poole?Wilson
Chapter five Lactic Acidosis within the mind: prevalence, Triggering Mechanisms and Pathophysiological value (pages 77–100): Bo okay. Siesjo
Chapter 6 Glutamine Metabolism in Metabolic Acidosis (pages 101–119): George A. O. Alleyne, Jose A. Lupianez, Norma McFarlane?Anderson, Paloma Hortelano, Jacqueline Benjamin, Jennifer Barnswell and Barbara Scott
Chapter 7 The law of Ketogenesis (pages 120–144): Daniel W. Foster and J. Denis McGarry
Chapter eight initial Observations at the Metabolic Responses to workout in people, utilizing 31?Phosphorus Nuclear Magnetic Resonance (pages 145–152): B. D. Ross, G. ok. Radda, D. G. Gadian, D. Taylor, P. Bore and P. Styles
Chapter nine Metabolic Acidosis and adjustments in Water and Electrolyte stability After Maximal workout (pages 153–167): Ole M. Sejersted, Jon I. Medbo and Lars Hermansen
Chapter 10 a few Hormonal impacts on Glucose and Ketone physique Metabolism in basic Human topics (pages 168–191): D. G. Johnston, A. Pernet, A. McCulloch, G. Blesa?Malpica, J. M. Burrin and ok. G. M. M. Alberti
Chapter eleven results of unfastened Fatty Acids, Insulin, Glucagon and Adrenaline on Ketone physique creation in people (pages 192–213): John M. Miles, Morey W. Haymond and John E. Gerich
Chapter 12 Quantitative points of L(+)?Lactate Metabolism in humans (pages 214–234): H. Connor and H. F. Woods
Chapter thirteen The function of Catecholamines in Metabolic Acidosis (pages 235–253): David S. Schade
Chapter 14 Acid?Base stability in Diabetic Ketoacidosis (pages 254–272): Leif Sestoft, Morten Folke, Paul D. Bartelst and Michael O. Marshall
Chapter 15 Isotope Turnover reviews in out of control Diabetes and the results of Insulin (pages 273–292): J. Saunders, M. A. Boroujerdi, P. M. Brown, E. R. Carsons, S. E. H. corridor, A. M. Umpleby and P. H. Sonksen
Chapter sixteen Metabolic Acidosis within the severely ailing (pages 293–306): H. J. G. Burns, B. N. Cowan and that i. McA. Ledingham
Chapter 17 The function of Altered Lactate Kinetics within the Pathogenesis of kind B Lactic Acidosis (pages 307–323): H. F. Woods, H. Connor and G. T. Tucker
Chapter 18 natural Acidurias: procedure, effects and medical Relevance (pages 324–339): S. ok. Wadman, M. Duran and J. P. Kamerling
Chapter 19 difficulties within the Congenital Lactic Acidoses (pages 340–371): J. V. Leonard
Chapter 20 Chairman's precis (pages 372–374): ok. G. M. M. Alberti
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Additional info for Ciba Foundation Symposium 87 - Metabolic Acidosis
Karger, Basel (International symposium on lactate in acute conditions) p 10-19 Halestrap AP 1976 Transport of pyruvate and lactate into human erythrocytes. Biochem J 156:193-207 Monson JP, Smith JA, Cohen RD, Iles RA 1981 Characterization of the hepatocyte plasma membrane transport mechanism for lactate. Clin Sci 60:4P-5P Pardridge WM, Oldendorff WH 1977 Transport of metabolic substrates through the blood-brain barrier. J Neurochem 285-12 Sestoft L, Kristensen L 0 1979 Determination of unidirectional fluxes of phosphate across plasma membrane in isolated perfused rat liver.
Subsequent work (Iles et a1 1977) showed that this effect was principally due to inhibition of gluconeogenesis from lactate at a step lying between pyruvate and oxaloacetate. This is also likely to be true for respiratory as well as metabolic acidosis (Iles et a1 1978). e. elevation of cytosol malate :oxaloacetate) by lowered cytosol pH. Interpretation of the measured fall in pHi was difficult, since although cytosol p H almost certainly fell (its contribution to pH measured by DMO being a major one, because of its large relative volume) it was, of course, not possible to determine the effect of acidosis on mitochondrial pH.
This is indicative of the great sensitivity of metabolic and transport processes in the kidney to extracellular H+ concentration. The important question of how intracellular renal pH responds to variations in extracellular pH is largely unsolved. e. there is a small gradient across the cell while the urine pH is close to that of the perfusate). 2 units could be present (Radda et a1 1980). Studies on isolated tubular cell preparations from the renal cortex, medulla and papilla do indeed show variations in intracellular pH between the different cell types.