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Metabolism
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
Energy is generated from metabolic fuels (carbohydrates, fats and proteins) and from reduced molecules, which are oxidized to release energy. Oxidation involves removing electrons at high potential from the fuel molecules and transferring them to a lower potential, thus releasing energy. The removed electrons must be transferred to a suitable electron acceptor, which has to be transportable, soluble in water and generally available. In cells, oxygen is the electron acceptor used. Unfortunately, oxygen is too reactive to be the immediate oxidizing agent and, so, intermediates, nicotinamide adenine dinucleotide (NAD+) and flavin adenine dinucleotide (FAD), are employed as carriers of electrons between the metabolic pathways and the site of oxygen consumption in mitochondria. NAD+ and FAD are reduced by the major metabolic pathways (e.g. glycolysis and citric acid (Krebs) cycle) to NADH + H+ and FADH2 and carry electrons to the electron transport chain. In the electron transport chain, the electrons are transferred through a series of carriers of lower potential until they finally combine with oxygen to form water. In this process, energy is released, and ATP is formed from adenosine diphosphate (ADP) by the process of oxidative phosphorylation (Figure 65.1).
Anti-platelet therapy in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Kunal Mahajan, Yashasvi Rajeev, K Sarat Chandra
Adenosine diphosphate (ADP), an important platelet agonist, has P2Y1 and P2Y12 receptors on the platelet plasma membrane through which it exerts its effects. Out of these two, it is the P2Y12 pathway that plays a major contribution in sustaining and stabilising the aggregation of platelets [10]. P2Y12 receptor antagonists are therefore recommended to prevent ischaemic events both in the acute and long-term treatment of ACS. The thienopyridine, ticlopidine, which was the first P2Y12 receptor inhibitor, is seldom prescribed now following the reports of serious adverse reactions with its use, particularly neutropenia and thrombotic thrombocytopenic purpura [11]. Three oral ADP P2Y12 receptors inhibiting drugs that are currently approved for clinical use include clopidogrel, prasugrel (irreversible inhibition), and ticagrelor (reversible inhibition) (Table 11.1).
Fetal Circulation
Published in Miriam Katz, Israel Meizner, Vaclav Insler, Fetal Well-Being, 2019
Miriam Katz, Israel Meizner, Vaclav Insler
Adequate oxygen supply is necessary for normal cellular metabolism and energy production. The mitochondria need oxygen for the synthesis of adenosine triphosphate (ATP). This is a high energy phosphate that by conversion into adenosine diphosphate (ADP) releases energy needed for the intracellular metabolism, and then returns to the mitochondria. This is a continuous process which normally goes in both directions at an equal rate, provided that oxygen supply is adequate. Hypoxia and accumulation of hydrogen ions will inhibit the production of ATP and cause profound changes in the intracellular metabolism.
Chronic exposure to dim artificial light disrupts the daily rhythm in mitochondrial respiration in mouse suprachiasmatic nucleus
Published in Chronobiology International, 2023
Prabha Rajput, Dhanananajay Kumar, Sairam Krishnamurthy
Mitochondrial respiration was assessed as previously described by (Rajput and Krishnamurthy 2022; Samaiya and Krishnamurthy 2015), with a Clark-type electrode in a sealed, thermostatically controlled chamber at 37°C. Briefly, the mitochondria were added to the respiratory chamber states were evaluated with suitable substrates and inhibitors. Purified mitochondrial protein was suspended in a respiration buffer in a final volume of 250 μL. State II respiration was initiated by adding pyruvate/malate; (P/M) shows a basal respiration rate. The addition of adenosine diphosphate-initiated state III respiration; (ADP); the high level of oxygen utilization indicates that ADP is converted into ATP. The addition of oligomycin measured state IV. The addition of FCCP measured state V. This causes uncoupling of the ETC to ATP synthesis and represents the maximum respiration rate. Rotenone was then added to shut down complex I-mediated respiration. The addition of succinate determined state V. This is the maximum respiration rate via complex II since FCCP is present. The RCR was calculated by dividing state III respiration (presence of ADP) by state IV respiration (absence of ADP).
Long-term survival of Icelandic women following acute myocardial infarction
Published in Scandinavian Cardiovascular Journal, 2022
Helga R. Gardarsdottir, Martin I. Sigurdsson, Karl Andersen, Ingibjorg J. Gudmundsdottir
Prior MI, percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) were recorded as defined in the database. Since these were AMI patients, they were all done urgently but it was also recorded whether they were done acutely as primary PCIs. The results of the coronary angiography were expressed as the number of vessels with significant stenoses or left main stem disease based on angiographic results with further physiological studies (IVUS or flow measurements) as deemed necessary by the operator. If PCI was performed, it was recorded whether patients received aspirin (acetylsalicylic acid) or an adenosine diphosphate receptor (ADP) inhibitor before or during the procedure. The choice of treatment, medical therapy alone, PCI or CABG, was at the discretion of the attending interventional cardiologist and/or the heart team.
Platelet surface GPIbα, activated GPIIb-IIIa, and P-selectin levels in adult veno-arterial extracorporeal membrane oxygenation patients
Published in Platelets, 2022
Michael Mazzeffi, Kenichi Tanaka, Yi-Feng Wu, Aijun Zhang, Niharika Kareddy, Emmanuel Tadjou Tito, Peter Rock, Alan D. Michelson, Andrew L. Frelinger
Within 30 minutes of collection, ECMO patient blood (20 uL) was added to four separate microtubes containing 1) PAC1-FITC plus 2 µg/mL eptifibatide (Millenium Pharmaceuticals, Cambridge, MA; eptifibatide blocks specific PAC1-FITC binding) irrelevant isotype-matched biotinylated antibody and HT buffer, 2) test antibody (PAC1 [activated GPIIb-IIIa-specific] conjugated with fluorescein isothiocyanate [FITC], CyFlow™, Sysmex Flow Cytometry, catalog # 1F145T100) and anti-P-selectin-biotin (clone AK4, CyFlow™ CD62P Biotin, Sysmex Flow Cytometry, catalog # CU508361) plus HEPES Tyrode’s (HT) buffer, 3) test antibody plus adenosine diphosphate (ADP)(5 µM final concentration) in HT buffer, and 4) test antibody plus thrombin receptor agonist peptide (TRAP)(10 µM, SFLLRN-amide, Bachem, Torrance, CA) in HT buffer. Microtubes were incubated for 15 minutes at room temperature. After incubation, 200 µL of fixative solution (1% formaldehyde, 10 mM HEPES, 0.15 M NaCl) was added to each microtube to stabilize the samples for analysis at the Center for Platelet Research Studies (CPRS). Samples were shipped to CPRS by overnight mail after preparation and initial fixation at UMMC. All samples were analyzed within 2 days of initial fixation. Separate stability studies demonstrated no change in platelet surface activated GPIIb-IIIa and P-selectin on unstimulated and TRAP stimulated normal donor platelets in samples fixed for up to 4 days prior to secondary staining and analysis.