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Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
The bicarbonate buffer system is a solution of carbonic acid and bicarbonate ions in the blood and is the primary buffering system. Carbonic acid (H2CO3) forms by the hydration of carbon dioxide and then dissociates into bicarbonate (HCO3–) and H+.In mammals, the bicarbonate system is found primarily within red blood cells and works quite well in maintaining pH because the lungs and kidneys constantly remove CO2, preventing equilibrium from being reached.If environmental alterations occur increasing pH, the kidneys can excrete HCO3–.
Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Normal metabolism produces acid, which must be buffered to prevent severe acidosis. The major soluble buffers are bicarbonate, phosphate ions, ammonia, proteins and bone, which can all combine with free hydrogen ions. The buffer systems are all in equilibrium with each other. In the bicarbonate buffer system, water and carbon dioxide combine and dissociate into hydrogen ions and bicarbonate ions (Figure 8.23). This reaction is catalysed by the enzyme carbonic anhydrase. As carbon dioxide is removed by the lungs, ventilation can affect acid–base status.
Basic Concepts of Acid–Base Physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The bicarbonate buffer system has a low pKa of 6.1 compared with its physiological pH of 7.4, and the concentrations of its components (CO2 and ) are not high. However, the bicarbonate system is the most important extracellular buffer because plasma CO2 can be quickly regulated by changes in pulmonary ventilation, and is regulated by reabsorption or excretion in the kidneys. The renal compensatory mechanisms occur slowly over several days.
Estimation of the risk of local and systemic effects in infants after ingestion of low-concentrated weak acids from descaling products
Published in Clinical Toxicology, 2022
Arjen Koppen, Claudine C. Hunault, Regina G. D. M. van Kleef, Agnes G. van Velzen, Remco H. S. Westerink, Irma de Vries, Dylan W. de Lange
Moreover, it is difficult to predict the occurrence of systemic effects after such exposures. In case of a functional intestinal barrier, the rate of acid absorption, metabolism and excretion determines the acid load. At a steady state, blood pH is tightly regulated and buffered, since protein function is strongly dependent on pH. Mechanisms for pH auto-regulation include the carbonic acid–bicarbonate buffer system, renal bicarbonate homeostasis, renal excretion of ammonium ions, respiratory control of the partial pressure of carbon dioxide and buffering by bone [6,7]. Systemic effects may occur when acids enter the blood circulation after ingestion of large amounts. Damage to the gastrointestinal barrier promotes the absorption of larger amounts of acids. In some cases, the resulting acidemia (lowering of blood pH) cannot be corrected sufficiently and symptoms like hemolysis, thrombocytopenia, clotting disorders, changes in respiratory rate, Kussmaul respiration, kidney disorders, nausea and vomiting can be observed [8].
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
The immediate buffering of H+ allows the pH to remain relatively stable in case of an acute acid load; however, without excretion of the net acid (50–100 meq/day) and reabsorption and regeneration of bicarbonate, the bicarbonate buffer system would not be sustainable since the body would quickly run out of bicarbonate. The kidneys play a vital role in these processes by excreting protons (mostly by titratable acidity and NH4+ excretion) and by reabsorbing and adding new bicarbonate to the body. Reabsorption of filtered bicarbonate occurs mainly through Na+/H+ exchange at the luminal membrane of the proximal tubule (80–90% of bicarbonate reabsorption).The net excretion of protons occurs by a process referred to as titratable acidity (main buffer = HPO42-) and by excretion of ammonium (see equation) [2]. Through ammonium excretion, new bicarbonate is added to the body. Under normal conditions, the net acid load of around 70 meq/day is excreted as 20–40 mmol of NH4+ and 30–50 mmol of H2PO4−. When the net acid load is increased, only NH4+ excretion can be sufficiently increased to excrete this extra acid because it does not take long for the HPO42- buffer system to get overwhelmed [1].
Simulated biological fluids – a systematic review of their biological relevance and use in relation to inhalation toxicology of particles and fibres
Published in Critical Reviews in Toxicology, 2021
Emma Innes, Humphrey H. P. Yiu, Polly McLean, William Brown, Matthew Boyles
As well as fluid composition, the pH of lung lining fluid is a parameter needing clarification. Although, the pH here is often considered near-neutral (pH 7.4) (Adamcakova-Dodd et al. 2014), there is not a set, or stable pH, as this environment is subject to change dependent of circumstance – during active host defence in the form of inflammation, for example (Ng et al. 2004), which would be the case if exogenous material was to reach the alveoli. In the upper respiratory tract the pH of the fluid lining has been measured in humans to be pH 6.6 via a bronchoscopy-associated pH probe, and pH 6.8 in excised tissue, and in exposed mouse trachea to be pH 6.9–7.1 (Bodem et al. 1983; Jayaraman et al. 2001a, 2001b). Although changes were shown to align with similar changes in blood pH (Jayaraman et al. 2001a), the mechanism of pH alteration has been assigned to release of H+ and/or HCO3− from bronchial epithelial cells (Lee et al. 1998; Coakley et al. 2003), in the already CO2-rich environment. Buffering of this fluid is thought to be obtained by secreted proteins such as mucin glycoproteins (Ng et al. 2004). In the alveolar space, the presence of alveolar macrophages is expected to influence the composition of the lung lining fluid and, being a source of high levels of H+, will impact greatly of alveolar fluid pH (Ng et al. 2004). Accurate measurements of alveolar pH are not easily obtained, but it has been suggested that this fluid is approximately pH 6.9 (Nielson et al. 1981). pH buffering within this environment is thought to be through a number of mechanisms including a CO2-bicarbonate buffer system (Kanapilly 1977) or the activity of surfactant proteins (Ng et al. 2004). Alveolar macrophages will, under resting conditions, release H+ at a rate of 2–3 nmol/min/106 cells, this is increased by up to 5 times when cells are activated (Bidani et al. 1989; Heming and Bidani 1995). So in the presence of inhaled materials, for example, when there is an increase in the cells’ metabolic activity and recruitment of further immune cells, it is possible that the increased release of H+ would reduce the localised pH (Ng et al. 2004). In addition to this, the environment surrounding activated macrophages would also be enriched with nitric oxide (NO) and other reactive nitrogen and oxygen species, as well as the secretions of recruited neutrophils, including further reactive oxygen species (ROS) as well as granule components (Tam et al. 2011).