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Metabolic Laboratory Data
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
The bicarbonate (HCO3) level is the other major anion in the circulation. While it is not a nutrient, its level is critical to the acid-base status. So, it has a great metabolic importance. Bicarbonate is a blood buffering system, acquiring excess H+ ions to form H2CO3, carbonic acid (CA). CA is then rapidly converted to H2O and CO2 by carbonic anhydrase. The CO2 is exhaled through the respiratory system and the water is eliminated in the urine or sweat. HCO3 is also eliminated directly from the distal nephron.
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Bicarbonate: Bicarbonate ions (HCO3−) are involved as an alkaline buffer to regulate and maintain pH balance in the extracellular blood plasma, while the serum level of bicarbonate lies between 22 and 30 mmol/L.127–130 However, ingested food, medication, chronic disease, or dehydration can increase system acidity, and consequently, bicarbonate levels can be increased to maintain the homeostatic equilibrium of an alkaline blood pH of 7.4.127–131
Biochemistry of Buffering Capacity and Ingestion of Buffers In Exercise and Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Bryan Saunders, Guilherme G. Artioli, Eimear Dolan, Rebecca L. Jones, Joseph Matthews, Craig Sale
Normal resting blood bicarbonate concentrations range between 23 and 27 mmol·L−1 (67). Sodium bicarbonate is a buffering agent capable of inducing alkalosis via increases in blood pH and bicarbonate (21, 60). This aids in the maintenance of muscle acid–base balance during exercise, increasing the efflux of H+ from the contracting muscle (59), forming carbonic acid, and allowing further buffering by the respiratory system (Figure 22.3). Sodium bicarbonate is another supplement included as one of the five sport supplements that have sufficient evidence to support their use by the International Olympic Committee (68).
Comparison of Centrifugal and Pulsatile Perfusion to Preserve Donor Kidneys Using Ex Vivo Subnormothermic Perfusion
Published in Journal of Investigative Surgery, 2022
Patrick P. W. Luke, Larry Jiang, Aushanth Ruthirakanthan, Daniel Lee, Qizhi Sun, Mahms Richard-Mohamed, Justin Kwong, Shahid Aquil, Rafid Alogaili, Aaron Haig, Alp Sener, Rabindra N. Bhattacharjee
Under general anesthesia, kidneys were subjected to 30 min warm ischemia in situ by cross-clamping the renal pedicles. After retrieval and flush with HTK solution, the paired kidneys were randomly assigned to undergo either: a) pulsatile perfusion or b) centrifugal perfusion with a hemoglobin oxygen carrier, HBOC-201, containing no vasodilators and nutrients at 22 °C. Oxygenation was achieved by an oxygenator and was set at 40%. Bicarbonate was added to adjust pH to physiologic levels. Urinary loss was replenished by equivalent volumes of PlasmaLyte solution (Baxter Corporation, USA) every half hour. A mean pressure of 70 mmHg was maintained during perfusion and perfusate oxygenation. Pump parameters such as flow rate and pressure were recorded every hour during preservation stage as well as reperfusion stage. After 4 hr perfusion with HBOC-201 at 22 °C, the function of both kidneys was assessed by reperfusion with autologous blood on pulsatile pump at 37 °C for another 4 hr to mimic post-storage transplantation conditions. Pump pressure, pH and oxygenation were maintained as if in perfusion. Blood pO2, pH and osmolality were monitored during reperfusion. To evaluate renal function, creatinine (10 mg/L) was added to the circuit. Figure 1B is a summary of the experimental procedure for our pump comparison.
Poisoning of glutaraldehyde-containing products: clinical characteristics and outcomes
Published in Clinical Toxicology, 2021
Suthimon Thumtecho, Charuwan Sriapha, Achara Tongpoo, Umaporn Udomsubpayakul, Winai Wananukul, Satariya Trakulsrichai
Systemic symptoms involved various systems and included abnormal vital signs, neurological symptoms, electrolyte imbalance and altered kidney function, liver function, and muscle enzymes. In some patients, oral exposure caused severe local effects, which might have produced and contributed to some of the systemic effects such as fever or tachycardia. Some patients experienced metabolic acidosis, low serum bicarbonate levels, or a wide anion gap. These findings were thought to result from an accumulation of glutaric acid, a GA metabolite [1,11]. Unfortunately, no metabolites were confirmed in this study. The resulting AKI might be explained by many factors including fluid loss from corrosive effects. Additionally, available animal data implied that the kidney is a target of toxicity following the oral administration of glutaraldehyde, although no human data were found to support this assumption [10]. Other systemic effects found in our study, including hepatitis and alteration of consciousness, have not been well documented as resulting from GA toxicity.
Difference between plasma and red blood cell acetone distribution during the first 60 h of a massive intoxication
Published in Clinical Toxicology, 2018
Matthieu Grégoire, Alain Pineau, Cédric Bretonnière, Joyce Niang, Karim Lakhal, Guillaume Deslandes
After a first episode of acetone intoxication six months earlier (1 L of acetone with plasma concentration at hospital admission of 3.7 g/L), a 55-year-old patient was hospitalized in intensive care because of coma (Glasgow Coma Scale [GCS] 3). He was currently prescribed quetiapine, levodopa, propranol, oxazepam, and domperidone for a Parkinson's disease associated with vestibular disorders and depressive syndrome. Brain CT-scan was non-contributory and an acute kidney injury (serum creatinine of 153 µmol/L on day 1) was not felt to be related to circulatory failure (heart rate 70/min, blood pressure 100/60 mmHg) but could have been an artifact due to interference of acetone with the creatinine dosage method (Jaffe reaction colorimetric kit, Roche, Basel, Switzerland). The blood pH was 7.36 with serum bicarbonate of 24.9 mmol/L. The patient was maintained on mechanical ventilation, slowly aroused and extubation was possible on day 4. He was discharged at his baseline neurological status and GCS 15.