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1

Pohjanvirta, Raimo. The AH receptor in biology and toxicology. Hoboken, N.J: Wiley, 2011.

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2

NATO Advanced Study Institute on Carbon Dioxide: Chemical and Biochemical Uses as a Source of Carbon (1986 Pugnochiuso, Italy). Carbon dioxide as a source of carbon: Biochemical and chemical uses. Dordrecht: D. Reidel Pub. Co., 1987.

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3

The slender thread: Web of life, the story of carbon dioxide. Corpus Christi: Helix Press, 1985.

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4

McKinney, Aubrey R. The slender thread: Web of life, the story of carbon dioxide. Corpus Christi, Tex: Helix Press, 1995.

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5

Thoene, Barbara. Untersuchungen zur Aufnahme und Metabolisierung atmosphärischen Stickstoffdioxyds in oberindischen Organen der Fichte (Picea abies (L.) Karst.). Frankfurt/M: Wissenschafts-Verlag W. Maraun, 1991.

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6

W, Ludden Paul, Burris John E e Burris Robert H. 1914-, eds. Nitrogen fixation and CO₂ metabolism: Proceedings of the Fourteenth Steenbock Symposium held 17-22 June 1984 at the University of Wisconsin--Madison, Madison, Wisconsin, U.S.A. New York: Elsevier, 1985.

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7

Ludden, P. W., e J. E. Burris. Nitrogen Fixation and Carbon Dioxide Metabolism. Elsevier, 1985.

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8

Nahas, G. Carbon Dioxide and Metabolic Regulations. Springer, 2011.

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9

Pohjanvirta, Raimo. AH Receptor in Biology and Toxicology. Wiley & Sons, Incorporated, John, 2011.

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10

Pohjanvirta, Raimo. AH Receptor in Biology and Toxicology. Wiley & Sons, Incorporated, John, 2011.

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11

Pohjanvirta, Raimo. AH Receptor in Biology and Toxicology. Wiley & Sons, Incorporated, John, 2011.

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12

Pohjanvirta, Raimo. Ah Receptor in Biology and Toxicology. Wiley & Sons, Incorporated, John, 2012.

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13

1919-, Tolbert N. E., e Preiss Jack 1932-, eds. Regulation of atmospheric C0₂ and 0₂ by photosynthetic carbon metabolism. New York: Oxford University Press, 1994.

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14

(Editor), M. Aresta, e G. Forti (Editor), eds. Carbon Dioxide as a Source of Carbon: Biochemical and Chemical Use (NATO Science Series C:). Springer, 1987.

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15

1934-, Brändén Carl-Ivar, Schneider Gunter e Kungl Svenska vetenskapsakademien, eds. Carbon dioxide fixation and reduction in biological and model systems: Proceedings of the Royal Swedish Academy of Sciences Nobel symposium, 1991. Oxford: Oxford University Press, 1994.

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16

Chakera, Aron, William G. Herrington e Christopher A. O’Callaghan. Disorders of acid–base balance. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0178.

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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.
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17

Ho, Kwok M. Kidney and acid–base physiology in anaesthetic practice. Editado por Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0005.

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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.
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18

Burton, Derek, e Margaret Burton. Excretion. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0008.

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Excretion is the removal of metabolic wastes such as ammonia, carbon dioxide, ions and water as well as toxic xenobiotics and metals. The process involves the gills, kidney, liver and rectal gland (elasmobranchs and coelacanth). In the liver, amino acids, haemoglobin, steroids and molecules resulting from human activities are transformed to excretable products. The rectal gland excretes ions, notably Na+ and Cl−. The kidney in teleosts has a distinction between an anterior head-kidney containing haematopoietic tissue and endocrine tissue and the posterior region with nephrons (kidney tubules). Fish nephrons generally have a Malphigian corpuscle with a glomerulus but the structure varies between fish taxa and some marine teleosts lack a glomerulus. Control systems for fish excretion are unclear but it is expected that various hormones influence excretory homeostasis.
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19

U, Sliwka, e United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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20

Jacobsen, Dean, e Olivier Dangles. Strategies and adaptations to aquatic life at high altitude. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198736868.003.0005.

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Chapter 5 is focused on how organisms cope with the environmental conditions that are a direct result of high altitude. Organisms reveal a number of fascinating ways of dealing with a life at high altitude; for example, avoidance and pigmentation as protection against damaging high levels of ultraviolet radiation, accumulation of antifreeze proteins, and metabolic cold adaptation among species encountering low temperatures with the risk of freezing, oxy-regulatory capacity in animals due to low availability of oxygen, and root uptake from the sediment of inorganic carbon by plants living in waters poor in dissolved carbon dioxide. These and more adaptations are carefully described through a number of examples from famous flagship species in addition to the less well-known ones. Harsh environmental conditions work as an environmental filter that only allows the well-adapted species to slip through to colonize high altitude waters.
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21

Joynt, Gavin M., e Gordon Y. S. Choi. Blood gas analysis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0072.

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Arterial blood gases allow the assessment of patient oxygenation, ventilation, and acid-base status. Blood gas machines directly measure pH, and the partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) dissolved in arterial blood. Oxygenation is assessed by measuring PaO2 and arterial blood oxygen saturation (SaO2) in the context of the inspired oxygen and haemoglobin concentration, and the oxyhaemoglobin dissociation curve. Causes of arterial hypoxaemia may often be elucidated by determining the alveolar–arterial oxygen gradient. Ventilation is assessed by measuring the PaCO2 in the context of systemic acid-base balance. A rise in PaCO2 indicates alveolar hypoventilation, while a decrease indicates alveolar hyperventilation. Given the requirement to maintain a normal pH, functioning homeostatic mechanisms result in metabolic acidosis, triggering a compensatory hyperventilation, while metabolic alkalosis triggers a compensatory reduction in ventilation. Similarly, when primary alveolar hypoventilation generates a respiratory acidosis, it results in a compensatory increase in serum bicarbonate that is achieved in part by kidney bicarbonate retention. In the same way, respiratory alkalosis induces kidney bicarbonate loss. Acid-base assessment requires the integration of clinical findings and a systematic interpretation of arterial blood gas parameters. In clinical use, traditional acid-base interpretation rules based on the bicarbonate buffer system or standard base excess estimations and the interpretation of the anion gap, are substantially equivalent to the physicochemical method of Stewart, and are generally easier to use at the bedside. The Stewart method may have advantages in accurately explaining certain physiological and pathological acid base problems.
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22

The Arterial Chemoreceptors. Springer, 2006.

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23

(Editor), Yoshiaki Hayashida, Constancio Gonzalez (Editor) e Hisatake Kondo (Editor), eds. The Arterial Chemoreceptors (Advances in Experimental Medicine and Biology). Springer, 2006.

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24

Kirchman, David L. Degradation of organic matter. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0007.

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The aerobic oxidation of organic material by microbes is the focus of this chapter. Microbes account for about 50% of primary production in the biosphere, but they probably account for more than 50% of organic material oxidization and respiration (oxygen use). The traditional role of microbes is to degrade organic material and to release plant nutrients such as phosphate and ammonium as well as carbon dioxide. Microbes are responsible for more than half of soil respiration, while size fractionation experiments show that bacteria are also responsible for about half of respiration in aquatic habitats. In soils, both fungi and bacteria are important, with relative abundances and activity varying with soil type. In contrast, fungi are not common in the oceans and lakes, where they are out-competed by bacteria with their small cell size. Dead organic material, detritus, used by microbes, comes from dead plants and waste products from herbivores. It and associated microbes can be eaten by many eukaryotic organisms, forming a detritus food web. These large organisms also break up detritus into small pieces, creating more surface area on which microbes can act. Microbes in turn need to use extracellular enzymes to hydrolyze large molecular weight compounds, which releases small compounds that can be transported into cells. Fungi and bacteria use a different mechanism, “oxidative decomposition,” to degrade lignin. Organic compounds that are otherwise easily degraded (“labile”) may resist decomposition if absorbed to surfaces or surrounded by refractory organic material. Addition of labile compounds can stimulate or “prime” the degradation of other organic material. Microbes also produce organic compounds, some eventually resisting degradation for thousands of years, and contributing substantially to soil organic material in terrestrial environments and dissolved organic material in aquatic ones. The relationship between community diversity and a biochemical process depends on the metabolic redundancy among members of the microbial community. This redundancy may provide “ecological insurance” and ensure the continuation of key biogeochemical processes when environmental conditions change.
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25

G, O'Regan R., e International Symposium on Arterial Chemoreceptors (12th : 1993 : Dublin, Ireland), eds. Arterial chemoreceptors: Cell to system. New York: Plenum Press, 1994.

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