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Carbon Dioxide Carriage in Blood
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
Carbon dioxide is produced in the mitochondria and diffuses down a partial pressure gradient into the interstitial fluid, across the capillary wall and into the plasma. Some dissolves in the plasma and some in the erythrocyte. Most of the carbon dioxide forms either carbamino compounds or bicarbonate (carbonic anhydrase) inside the erythrocyte. As oxygen is also moving out of the erythrocyte into the tissues, the storage of carbon dioxide is enhanced by the increased buffering of hydrogen ions by deoxygenated or reduced haemoglobin (HHb) released from carbonic acid, thus allowing increased bicarbonate production and the formation of carbamino haemoglobin (HbNHCOOH). Bicarbonate ions diffuse out of the cell (hydrogen ions cannot do this and must be buffered inside the erythrocyte) and, to maintain electrical neutrality, chloride ions diffuse into the cell – as does water (Figure 19.2). This is called the chloride shift or Hamberger effect.
Haematology and Immunology
Published in Sarah Armstrong, Barry Clifton, Lionel Davis, Primary FRCA in a Box, 2019
Sarah Armstrong, Barry Clifton, Lionel Davis
RBCs contain haemoglobin and the enzyme carbonic anhydraseCarbonic anhydrase catalyzes the formation of H+ and from carbon dioxide produced in the tissuesThe bicarbonate formed diffuses into the plasma in exchange for chloride (chloride shift)In the lungs, the opposite occurs to release carbon dioxide
The respiratory system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
The carbon dioxide produced during cellular metabolism diffuses out of the cells and into the plasma. It then continues to diffuse down its concentration gradient into the red blood cells. Within the red blood cells, the enzyme, carbonic anhydrase (CA), facilitates the combination of carbon dioxide and water to form carbonic acid (H2CO3). The carbonic acid then dissociates into hydrogen ion (H+) and bicarbonate ion (HCO3−). As the bicarbonate ions are formed, they diffuse down their concentration gradient out of the red blood cell and into the plasma. This process is beneficial because bicarbonate ion is far more soluble in the plasma than carbon dioxide. As the negatively charged bicarbonate ions exit the red blood cell, chloride ions, the most abundant anions in the plasma, enter the cells by way of HCO3−-Cl− carrier proteins. This process, referred to as the chloride shift, maintains electrical neutrality. Many of the hydrogen ions bind with hemoglobin. As with carbon dioxide, deoxyhemoglobin can bind more readily with hydrogen ions than oxygenated hemoglobin.
Expression of Na/K-ATPase subunits in the human cochlea: a confocal and super-resolution microscopy study with special reference to auditory nerve excitation and cochlear implantation
Published in Upsala Journal of Medical Sciences, 2019
Wei Liu, Maria Luque, Rudolf Glueckert, Niklas Danckwardt-Lillieström, Charlotta Kämpfe Nordström, Anneliese Schrott-Fischer, Helge Rask-Andersen
In the brain, astrocytes control osmotic equilibrium by modulating the activity of Na/K-ATPase via Ca2+ signaling (43) and chloride shift (44). Human spiral ganglion cell bodies are surrounded by a communicating glial syncytium (45), which may act similarly to maintain ion gradients across the plasma membrane after depolarization and neuron excitation. Our results suggest that the principal heterodimer in the human auditory nerve is α3β1, while in the satellite glial cells it is α1. The β isoform could not be unequivocally established, but it is assumed to be β2 with no β1 expression in the satellite glial cells; β2 is believed to be a homologue of the adhesion molecule on glia (AMOG) (46) and is said to be the principal β isoform in Schwann cells containing either α1β2 or α2β2 heterodimers (47). Watts et al. (48) found transcripts encoding the β1 subunit in neurons, while β2 subunit mRNA expression was characteristic of glia. Alfa2 subunit mRNA was typical for glia. A transcript of α3 subunit was found in neurons, while the α1 gene was present in all cell types in the rat brain (48). Their results suggest that that there may be more than one α subunit expressed within a single cell type.
From omics technologies to personalized transfusion medicine
Published in Expert Review of Proteomics, 2019
Significant drops in the intracellular and extracellular pH are observed during storage, a phenomenon mostly driven by impaired ion homeostasis and ongoing glycolytic metabolism – the only energy-generating pathway in mature red cells, owing to the lack of mitochondria [42,43]. Application of metabolomics tools in the field of transfusion medicine has allowed to define a decline in glycolytic rates as storage progresses [14,44,45]. This decline is observed at different rates during storage in all currently licensed storage additives, including SAGM [36,43,46,47], additive solutions 1 [48], 3 [45,49], 5 [50], and PAGGSM [51,52]. To counteract this phenomenon, strategies have been envisaged to leverage the chloride shift (and Donnan equilibrium) to promote the intracellular alkalinization of stored red blood cells and thus favor glycolysis. These strategies involve the design of low chloride or chloride free, bicarbonate loaded storage additives, which indeed boost glycolysis and energy metabolism in stored red blood cells and slow down the decline in ATP and DPG levels observed when erythrocytes are stored with currently marketed additives [51,53–55]. ATP synthesis is fueled by purines in the storage media, such as adenine, which is quickly consumed during the first 10–14 days of storage, though its repletion after storage week 2 does not provide significant benefits in terms of ATP synthesis capacity [56]. The take-home message from these studies is that (i) the progression of the metabolic lesion is comparable across storage additives, to such an extent that metabolic markers of the metabolic age of stored red cells can be easily defined [57–59]; (ii) however, the onset, severity, and extent of the metabolic lesion to energy metabolism is dependent on storage additives, which impact the metabolic heterogeneity of stored red cells to an extent comparable to the storage age itself, as a large scale, metabolomics study on ~600 samples seems to suggest (>10% of the total variance) [60].