Carbonic Anhydrase Inhibitors
Kidney Tubules, Distal
Acidosis, Renal Tubular
Carbonic Anhydrase II
Kidney Tubules, Proximal
Anion Transport Proteins
Biological Transport, Active
Rats, Inbred Strains
Loop of Henle
Kidney Tubules, Collecting
Peritoneal Dialysis, Continuous Ambulatory
Anion Exchange Protein 1, Erythrocyte
A kinetic study of ribulose bisphosphate carboxylase from the photosynthetic bacterium Rhodospirillum rubrum. (1/3033)The activation kinetics of purified Rhodospirillum rubrum ribulose bisphosphate carboxylase were analysed. The equilibrium constant for activation by CO(2) was 600 micron and that for activation by Mg2+ was 90 micron, and the second-order activation constant for the reaction of CO(2) with inactive enzyme (k+1) was 0.25 X 10(-3)min-1 . micron-1. The latter value was considerably lower than the k+1 for higher-plant enzyme (7 X 10(-3)-10 X 10(-3)min-1 . micron-1). 6-Phosphogluconate had little effect on the active enzyme, and increased the extent of activation of inactive enzyme. Ribulose bisphosphate also increased the extent of activation and did not inhibit the rate of activation. This effect might have been mediated through a reaction product, 2-phosphoglycolic acid, which also stimulated the extent of activation of the enzyme. The active enzyme had a Km (CO2) of 300 micron-CO2, a Km (ribulose bisphosphate) of 11--18 micron-ribulose bisphosphate and a Vmax. of up to 3 mumol/min per mg of protein. These data are discussed in relation to the proposed model for activation and catalysis of ribulose bisphosphate carboxylase. (+info)
NaCl-induced renal vasoconstriction in salt-sensitive African Americans: antipressor and hemodynamic effects of potassium bicarbonate. (2/3033)In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9+/-3.5 (mean+/-SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (DeltaMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920+/-75 to 828+/-46 (P<0.05); filtration fraction (FF, %) increased from 19. 4+/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (10(3)xmm Hg/[mL/min]) increased from 101+/-8 to 131+/-10 (P<0.001). In all subjects combined, DeltaMAP varied inversely with DeltaRBF (r =-0.57, P=0.02) and directly with DeltaRVR (r = 0.65, P=0.006) and DeltaFF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity. (+info)
Indirect evidence for cholinergic inhibition of intestinal bicarbonate absorption in humans. (3/3033)BACKGROUND: The aim of the study was to test the hypothesis that in the fasting state, proximal intestinal HCO3- absorption, which depends on villus Na+/H+ exchanger activity, is tonically inhibited by a cholinergic atropine sensitive mechanism. SUBJECTS: The experiments were performed in 34 healthy volunteers and in eight patients with intestinal villus atrophy. METHODS: HCO3- absorption was measured with a modified triple lumen perfusion technique in the distal duodenum, the most proximal portion of the small intestine. The study was designed to compensate for the inhibitory effects of atropine on intestinal motor activity. RESULTS: Atropine had three effects on HCO3- transport: it reduced HCO3- concentration at the proximal aspiration site, it displaced the relation between HCO3- concentration and HCO3- absorption to the left, and it induced a significant acidification of the perfusate at the distal aspiration site. The magnitude of the stimulatory effect on HCO3- absorption was similar to the difference between patients with intestinal villus atrophy and healthy controls. CONCLUSION: The data suggest that, in the fasting state, duodenal HCO3- absorption, which depends on villus Na+/H+ exchanger activity, may be tonically inhibited by an atropine sensitive cholinergic mechanism. (+info)
Role of a novel photosystem II-associated carbonic anhydrase in photosynthetic carbon assimilation in Chlamydomonas reinhardtii. (4/3033)Intracellular carbonic anhydrases (CA) in aquatic photosynthetic organisms are involved in the CO2-concentrating mechanism (CCM), which helps to overcome CO2 limitation in the environment. In the green alga Chlamydomonas reinhardtii, this CCM is initiated and maintained by the pH gradient created across the chloroplast thylakoid membranes by photosystem (PS) II-mediated electron transport. We show here that photosynthesis is stimulated by a novel, intracellular alpha-CA bound to the chloroplast thylakoids. It is associated with PSII on the lumenal side of the thylakoid membranes. We demonstrate that PSII in association with this lumenal CA operates to provide an ample flux of CO2 for carboxylation. (+info)
Topology of the membrane domain of human erythrocyte anion exchange protein, AE1. (5/3033)Anion exchanger 1 (AE1) is the chloride/bicarbonate exchange protein of the erythrocyte membrane. By using a combination of introduced cysteine mutants and sulfhydryl-specific chemistry, we have mapped the topology of the human AE1 membrane domain. Twenty-seven single cysteines were introduced throughout the Leu708-Val911 region of human AE1, and these mutants were expressed by transient transfection of human embryonic kidney cells. On the basis of cysteine accessibility to membrane-permeant biotin maleimide and to membrane-impermeant lucifer yellow iodoacetamide, we have proposed a model for the topology of AE1 membrane domain. In this model, AE1 is composed of 13 typical transmembrane segments, and the Asp807-His834 region is membrane-embedded but does not have the usual alpha-helical conformation. To identify amino acids that are important for anion transport, we analyzed the anion exchange activity for all introduced cysteine mutants, using a whole cell fluorescence assay. We found that mutants G714C, S725C, and S731C have very low transport activity, implying that this region has a structurally and/or catalytically important role. We measured the residual anion transport activity after mutant treatment with the membrane-impermeant, cysteine-directed compound, sodium (2-sulfonatoethyl)methanethiosulfonate) (MTSES). Only two mutants, S852C and A858C, were inhibited by MTSES, indicating that these residues may be located in a pore-lining region. (+info)
Modulation of chloride, potassium and bicarbonate transport by muscarinic receptors in a human adenocarcinoma cell line. (6/3033)1. Short-circuit current (I(SC)) responses to carbachol (CCh) were investigated in Colony 1 epithelia, a subpopulation of the HCA-7 adenocarcinoma cell line. In Krebs-Henseleit (KH) buffer, CCh responses consisted of three I(SC) components: an unusual rapid decrease (the 10 s spike) followed by an upward spike at 30 s and a slower transient increase (the 2 min peak). This response was not potentiated by forskolin; rather, CCh inhibited cyclic AMP-stimulated I(SC). 2. In HCO3- free buffer, the decrease in forskolin-elevated I(SC) after CCh was reduced, although the interactions between CCh and forskolin remained at best additive rather than synergistic. When Cl- anions were replaced by gluconate, both Ca2+- and cyclic AMP-mediated electrogenic responses were significantly inhibited. 3. Basolateral Ba2+ (1-10 mM) and 293B (10 microM) selectively inhibited forskolin stimulation of I(SC), without altering the effects of CCh. Under Ba2+- or 293B-treated conditions, CCh responses were potentiated by pretreatment with forskolin. 4. Basolateral charybdotoxin (50 nM) significantly increased the size of the 10 s spike of CCh responses in both KH and HCO3- free medium, without affecting the 2 min peak. The enhanced 10 s spike was inhibited by prior addition of 5 mM apical Ba2+. Charybdotoxin did not affect forskolin responses. 5. In epithelial layers prestimulated with forskolin, the muscarinic antagonists atropine and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, both at 100 nM) abolished subsequent 10 microM CCh responses. Following addition of p-fluoro hexahydro-sila-difenidol (pF-HHSiD, 10 microM) or pirenzepine (1 microM), qualitative changes in the CCh response time-profile also indicated a rightward shift of the agonist concentration-response curve; however, 1 microM gallamine had no effect. These results suggest that a single M3-like receptor subtype mediates the secretory response to CCh. 6. It is concluded that CCh and forskolin activate discrete populations of basolateral K+ channels gated by either Ca2+ or cyclic AMP, but that the Cl- permeability of the apical membrane may limit their combined effects on electrogenic Cl- secretion. In addition, CCh activates a Ba2+-sensitive apical K+ conductance leading to electrogenic K+ transport. Both agents may also modulate HCO3- secretion through a mechanism at least partially dependent on carbonic anhydrase. (+info)
Formal analysis of electrogenic sodium, potassium, chloride and bicarbonate transport in mouse colon epithelium. (7/3033)1. The mammalian colonic epithelium carries out a number of different transporting activities simultaneously, of which more than one is increased following activation with a single agonist. These separate activities can be quantified by solving a set of equations describing these activities, provided some of the dependent variables can be eliminated. Using variations in the experimental conditions, blocking drugs and comparing wild type tissues with those from transgenic animals this has been achieved for electrogenic ion transporting activity of the mouse colon. 2. Basal activity and that following activation with forskolin was measured by short circuit current in isolated mouse colonic epithelia from normal and cystic fibrosis (CF) mice. 3. Using amiloride it is shown that CF colons show increased electrogenic sodium absorption compared to wild type tissues. CF mice had elevated plasma aldosterone, which may be responsible for part or all of the increased sodium absorbtion in CF colons. 4. The derived values for electrogenic chloride secretion and for electrogenic potassium secretion were increased by 13 and 3 fold respectively by forskolin, compared to basal state values for these processes. 5. The loop diuretic, frusemide, completely inhibited electrogenic potassium secretion, but apparently only partially inhibited electrogenic chloride secretion. However, use of bicarbonate-free solutions and acetazolamide reduced the frusemide-resistant current, suggesting that electrogenic bicarbonate secretion accounts for the frusemide-resistant current. 6. It is argued that the use of tissues from transgenic animals is an important adjunct to pharmacological analysis, especially where effects in tissues result in the activation of more than one sort of response. (+info)
A novel role for carbonic anhydrase: cytoplasmic pH gradient dissipation in mouse small intestinal enterocytes. (8/3033)1. The spatial and temporal distribution of intracellular H+ ions in response to activation of a proton-coupled dipeptide transporter localized at the apical pole of mouse small intestinal isolated enterocytes was investigated using intracellular carboxy-SNARF-1 fluorescence in combination with whole-cell microspectrofluorimetry or confocal microscopy. 2. In Hepes-buffered Tyrode solution, application of the dipeptide Phe-Ala (10 mM) to a single enterocyte reduced pHi locally in the apical submembranous space. After a short delay (8 s), a fall of pHi occurred more slowly at the basal pole. 3. In the presence of CO2/HCO3--buffered Tyrode solution, the apical and basal rates of acidification were not significantly different and the time delay was reduced to 1 s or less. 4. Following application of the carbonic anhydrase inhibitor acetazolamide (100 microM) in the presence of CO2/HCO3- buffer, addition of Phe-Ala once again produced a localized apical acidification that took 5 s to reach the basal pole. Basal acidification was slower than at the apical pole. 5. We conclude that acid influx due to proton-coupled dipeptide transport can lead to intracellular pH gradients and that intracellular carbonic anhydrase activity, by facilitating cytoplasmic H+ mobility, limits their magnitude and duration. (+info)
There are several types of alkalosis, including:
1. Respiratory alkalosis: This type is caused by an excessive breathing of carbon dioxide into the lungs, which increases the bicarbonate levels in the blood.
2. Metabolic alkalosis: This type is caused by a decrease in the production of acid in the body, such as in diabetic ketoacidosis or liver disease.
3. Inherited alkalosis: This type is caused by inherited genetic disorders that affect the regulation of acid-base homeostasis.
4. Drug-induced alkalosis: Certain medications, such as antacids and diuretics, can increase bicarbonate levels in the blood.
5. Post-operative alkalosis: This type can occur after surgery, particularly gastrointestinal surgery, due to the release of bicarbonate from damaged tissues.
The symptoms of alkalosis can vary depending on the severity and duration of the condition. They may include:
* Nausea and vomiting
* Abdominal pain
* Muscle weakness
* Tingling sensations in the extremities
* Confusion and disorientation
If left untreated, alkalosis can lead to more severe complications such as:
* Respiratory acidosis (a decrease in blood pH due to a lack of oxygen)
* Cardiac arrhythmias (irregular heartbeats)
Diagnosis of alkalosis is based on a combination of physical examination, medical history, and laboratory tests. Laboratory tests may include:
* Arterial blood gas (ABG) analysis to measure the pH and PCO2 levels in the blood
* Serum electrolyte levels to assess the levels of sodium, potassium, and chloride
* Urine testing to assess the levels of bicarbonate and other electrolytes
Treatment of alkalosis depends on the underlying cause and severity of the condition. General measures may include:
* Correction of any underlying metabolic disorders, such as diabetes or kidney disease
* Discontinuation of medications that may be contributing to the alkalosis
* Fluid and electrolyte replacement to correct dehydration or imbalances
* Oxygen therapy to treat respiratory acidosis
In severe cases, hospitalization may be necessary to monitor and treat the condition. In some cases, medications such as sodium bicarbonate may be prescribed to help restore acid-base balance. Surgery may be required in cases where the alkalosis is caused by a structural problem, such as a hiatal hernia.
Prognosis for alkalosis depends on the underlying cause and severity of the condition. In general, early diagnosis and treatment can improve outcomes. However, untreated severe alkalosis can lead to complications such as seizures, coma, and cardiac arrhythmias.
Prevention of alkalosis involves identifying and treating underlying conditions that may contribute to the development of the condition. This includes managing chronic diseases such as diabetes and kidney disease, and avoiding medications that may cause alkalosis. Additionally, maintaining a balanced diet and staying hydrated can help prevent electrolyte imbalances that can lead to alkalosis.
In conclusion, alkalosis is a condition characterized by an excess of base in the body, which can lead to respiratory and metabolic disturbances. The diagnosis of alkalosis is based on a combination of physical examination, medical history, and laboratory tests. Treatment depends on the underlying cause and severity of the condition, and may include fluid and electrolyte replacement, medication, and addressing any underlying conditions. Early diagnosis and treatment can improve outcomes for patients with alkalosis.
There are several types of acidosis, including:
1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.
The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching
If left untreated, acidosis can lead to complications such as:
1. Kidney damage
4. Heart arrhythmias
5. Respiratory failure
Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:
1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.
In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.
Some common symptoms of respiratory acidosis include:
* Rapid breathing rate
* Shallow breathing
* Confusion or disorientation
* Muscle weakness
* Numbness or tingling in the hands and feet
If left untreated, respiratory acidosis can lead to serious complications such as seizures, coma, and even death. Treatment typically involves addressing the underlying cause of the condition, such as surgery for a weakened diaphragm or other breathing muscles, or using mechanical ventilation if necessary.
It is important to seek medical attention if you experience any symptoms of respiratory acidosis, as early diagnosis and treatment can help prevent complications and improve outcomes.
There are two main types of acid-base imbalances:
1. Respiratory acidosis: This occurs when the body produces too much carbon dioxide, leading to an increase in blood acidity. Causes include chronic obstructive pulmonary disease (COPD), pneumonia, and sleep apnea.
2. Metabolic acidosis: This occurs when the body produces too little base, leading to an increase in blood acidity. Causes include diabetic ketoacidosis, kidney failure, and excessive alcohol consumption.
Symptoms of acid-base imbalance can include:
* Coma (in severe cases)
Treatment of acid-base imbalance depends on the underlying cause and may involve corrective measures such as:
* Oxygen therapy
* Medications to restore blood pH balance
* Diuretics to remove excess fluids
* Insulin therapy (for metabolic acidosis)
* Hemodialysis (for severe cases of metabolic acidosis)
It is important for healthcare professionals to monitor and maintain acid-base balance in patients, particularly those with pre-existing medical conditions or those undergoing surgical procedures.
Respiratory alkalosis can occur due to various causes such as hypoventilation (breathing too slowly), hypercapnia (excessive carbon dioxide in the blood), bicarbonate therapy, or drinking excessive amounts of antacids. Symptoms may include vomiting, abdominal pain, headache, and muscle weakness.
Treatment typically involves addressing the underlying cause, such as correcting hypoventilation or removing excess carbon dioxide from the bloodstream. In severe cases, medications or mechanical ventilation may be necessary.
There are several types of RTA, including:
1. Type 1 RTA: This is caused by a defect in the genes that code for the proteins involved in acid secretion in the renal tubules.
2. Type 2 RTA: This is caused by damage to the renal tubules, such as from exposure to certain drugs or toxins.
3. Type 4 RTA: This is caused by a deficiency of the hormone aldosterone, which helps regulate electrolyte levels in the body.
Symptoms of RTA can include:
* Nausea and vomiting
* Abdominal pain
* Increased heart rate
* Decreased urine production
RTA can be diagnosed through blood tests that measure the pH levels in the body, as well as tests that assess kidney function and electrolyte levels. Treatment for RTA typically involves correcting any underlying causes, such as stopping certain medications or addressing electrolyte imbalances. In some cases, medications may be prescribed to help regulate acid levels in the body.
Prevention of RTA includes maintaining proper hydration, avoiding exposure to harmful substances, and managing any underlying medical conditions that may increase the risk of developing RTA. Early detection and treatment can help prevent complications and improve outcomes for individuals with RTA.
Symptoms of DKA can include:
* High blood sugar levels (usually above 300 mg/dL)
* High levels of ketones in the blood and urine
* Nausea, vomiting, and abdominal pain
* Fatigue, weakness, and confusion
* Headache and dry mouth
* Flu-like symptoms, such as fever, chills, and muscle aches
If left untreated, DKA can lead to serious complications, such as:
* Dehydration and electrolyte imbalances
* Seizures and coma
* Kidney damage and failure
Treatment of DKA typically involves hospitalization and intravenous fluids to correct dehydration and electrolyte imbalances. Insulin therapy is also started to lower blood sugar levels and promote the breakdown of ketones. In severe cases, medications such as sodium bicarbonate may be given to help neutralize the excess ketones in the blood.
Preventing DKA involves proper management of diabetes, including:
* Taking insulin as prescribed and monitoring blood sugar levels regularly
* Maintaining a healthy diet and exercise program
* Monitoring for signs of infection or illness, which can increase the risk of DKA
Early detection and treatment of DKA are critical to preventing serious complications and improving outcomes for people with diabetes.
Example sentence: "The patient was diagnosed with lactic acidosis secondary to uncontrolled diabetes and was admitted to the intensive care unit for proper management."
The normal range for potassium levels in the blood varies depending on age, gender, and other factors, but generally it is between 3.5 and 5.5 mEq/L (milliequivalents per liter).
Hypokalemia can be caused by a variety of factors such as diarrhea, vomiting, certain medications (diuretics, laxatives), kidney disease or malfunctioning of the parathyroid glands.
Intravenous sodium bicarbonate
Bicarbonate buffer system
Sodium bicarbonate rocket
Sodium bicarbonate cotransporter 3
Electrogenic sodium bicarbonate cotransporter 1
Electrogenic sodium bicarbonate cotransporter 4
Electroneutral sodium bicarbonate exchanger 1
Sodium bicarbonate transporter-like protein 11
List of inorganic compounds
List of unproven and disproven cancer treatments
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Sodium Bicarbonate Injection3
- Sodium Bicarbonate Injection, USP is a sterile, nonpyrogenic, hypertonic solution of sodium bicarbonate (NaHCO 3 ) in water for injection for administration by the intravenous route as an electrolyte replenisher and systemic alkalizer. (nih.gov)
- Sodium Bicarbonate Injection, USP is indicated in the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. (nih.gov)
- Sodium Bicarbonate Injection, USP is contraindicated in patients who are losing chloride by vomiting or from continuous gastrointestinal suction, and in patients receiving diuretics known to produce a hypochloremic alkalosis. (nih.gov)
- Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis. (nih.gov)
- But since an appreciable time interval may elapse before all of the ancillary effects are brought about, bicarbonate therapy is indicated to minimize risks inherent to the acidosis itself. (nih.gov)
- Vigorous bicarbonate therapy is required in any form of metabolic acidosis where a rapid increase in plasma total CO 2 content is crucial - e.g., cardiac arrest, circulatory insufficiency due to shock or severe dehydration, and in severe primary lactic acidosis or severe diabetic acidosis. (nih.gov)
- These images are a random sampling from a Bing search on the term "Sodium Bicarbonate in Severe Metabolic Acidosis. (fpnotebook.com)
- Because of the potential harms of acidemia, some clinicians still advocate for the use of bicarbonate in severe metabolic acidosis, generally defined as an arterial pH less than 7.15. (medscape.com)
- [ 34 , 35 ] It has been proposed that any improvement in hemodynamic status when bicarbonate is administered may be caused by mechanisms other than correction of acidosis (eg, increased preload, effect of tonicity). (medscape.com)
- Renal tubular acidosis (RTA) occurs when the kidneys are unable to maintain normal acid-base homeostasis because of tubular defects in acid excretion or bicarbonate ion reabsorption. (nih.gov)
- Proximal renal tubular acidosis (pRTA) is a syndrome caused by abnormal proximal tubule reabsorption of bicarbonate resulting in metabolic acidosis . (bvsalud.org)
- Studies have shown that low or high serum bicarbonate levels (reflecting metabolic acidosis or alkalosis) are associated with increased all-cause mortality rates in moderate and advanced chronic kidney disease (CKD) cases. (nih.gov)
- Correction of presumed acidosis using sodium bicarbonate, targeting serum levels around 22 mmol/L, has proven to be beneficial in delaying the progression of the disease and provided mortality benefit. (nih.gov)
- Bicarbonate anion is considered "labile" since at a proper concentration of hydrogen ion (H + ) it may be converted to carbonic acid (H 2 CO 3 ) and thence to its volatile form, carbon dioxide (CO 2 ) excreted by the lung. (nih.gov)
- Normally a ratio of 1:20 (carbonic acid: bicarbonate) is present in the extracellular fluid. (nih.gov)
- Total CO2 = bicarbonate + CO2 + carbonic acid. (loinc.org)
- Under normal circumstances, bicarbonate is the primary constituent of total CO2, however, in certain pathologic conditions, CO2 and/or carbonic acid contribute a clinically significant fraction of the total. (loinc.org)
- Sodium bicarbonate buffers lactic acid by essentially prolonging lactic acid build-up. (stack.com)
- Together with pH determination, bicarbonate measurements are used in the diagnosis and treatment of numerous potentially serious disorders associated with acid-base imbalance in the respiratory and metabolic systems. (cdc.gov)
- Sodium bicarbonate in water dissociates to provide sodium (Na + ) and bicarbonate (HCO 3 ¯ ) ions. (nih.gov)
- This protein transports negatively charged particles ( ions ), including chloride, iodide, and bicarbonate , into and out of cells. (nih.gov)
- Bicarbonate ions neutralize hydrogen ions and raise urinary and blood pH. (medscape.com)
- Sodium Bicarbonate, USP is chemically designated NaHCO 3 , a white crystalline powder soluble in water. (nih.gov)
- The effects of sodium bicarbonate (NaHCO 3 ) on anaerobic and aerobic capacity are commonly acknowledged as unclear due to the contrasting evidence thus, the present study analyzes the contribution of NaHCO 3 to energy metabolism during exercise. (biomedcentral.com)
- water and produces a negatively charged bicarbonate molecule ( bicarbonate ion ) and a positively charged hydrogen atom (known as a proton). (nih.gov)
- Calcium bicarbonate has been used as a neutralization and alkalization agent (AIC Book and Paper Catalog). (mfa.org)
- Effect of Bicarbonate, Calcium, and pH on the Reactivity of As(V) and U(VI) Mixtures. (nih.gov)
- Bicarbonate and calcium (Ca) can have major impacts on U speciation and can affect the reactivity between U and As. (nih.gov)
- Based on this function, AE1 is known as a chloride/ bicarbonate exchanger (Cl-/HCO3- exchanger). (nih.gov)
- The proposed study is a double blind, randomized, placebo-controlled, parallel-group trial in which 138 men and 138 women, age 60 and older, will take potassium bicarbonate in doses of 1.0 or 1.5 mmol/kg of body weight or placebo daily for three months. (nih.gov)
- We therefore investigated the reactivity of aqueous U and As mixtures with bicarbonate and Ca for acidic and neutral pH conditions. (nih.gov)
- Bicarbonate is an electrolyte and typically measured along with other electrolytes (e.g. sodium, potassium, and chloride) to detect, evaluate, and monitor electrolyte imbalances. (loinc.org)
- sodium bicarbonate iv , aspirin-dipyridamole oral Mechanism: passive renal tubular reabsorption due to increased pH. (rxlist.com)
- Tris-hydroxylmethyl aminomethane ( tromethamine [THAM]) is a buffering agent that does not generate carbon dioxide, which confers a theoretical benefit over sodium bicarbonate. (medscape.com)
- In our recently completed NIH-funded trial in 171 older men and women, alkalinizing the diet with a bicarbonate supplement daily for 3 months significantly reduced urinary excretion of N-telopeptide (NTX), a marker of bone resorption, and urinary nitrogen, a marker of muscle wasting. (nih.gov)
- The proposed dose-finding study will extend our previous work in this area by evaluating the effects of placebo and two doses of bicarbonate on urinary NTX and nitrogen excretion and on lower extremity performance. (nih.gov)
- Your doctor also may prescribe sodium bicarbonate to make your blood or urine less acidic in certain conditions. (medlineplus.gov)
- Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. (nih.gov)
- Bicarbonate is a simple single carbon molecule that plays surprisingly important roles in diverse biological processes. (nih.gov)
- Sodium bicarbonate also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. (nih.gov)
- model of chemotherapy-induced peripheral neuropathy in mice: use of vitamin C and sodium bicarbonate pretreatments to reduce nephrotoxicity and improve animal health status. (rndsystems.com)
- This research shows that adding sodium bicarbonate could improve the efficacy of creatine. (stack.com)
- However, two randomized, controlled trials comparing the effects of bicarbonate versus normal saline on critically ill patients requiring vasopressors demonstrated no improvement in hemodynamics with bicarbonate. (medscape.com)
- Low bicarbonate levels may occur in patients with Addison's disease, chronic diarrhea, diabetic ketoacidosis, and kidney disease. (loinc.org)
- Patients with mutations to the SLC4A4 gene ( coding for the sodium bicarbonate cotransporter NBCe1), have pRTA, growth delay, ocular defects, and enamel abnormalities . (bvsalud.org)
- Effect of sodium bicarbonate on functional outcome in patients with out-of-hospital cardiac arrest: a post-hoc analysis of a French and North-American dataset. (nih.gov)
- BACKGROUND AND IMPORTANCE: No large randomised controlled trial has assessed the potential benefits on neurologic outcomes of prehospital sodium bicarbonate administration in patients with nontraumatic out-of-hospital cardiac arrest (OHCA). (nih.gov)
- MAIN RESULTS: In the French dataset, of the 54 807 patients, 1234 (2.2%) received sodium bicarbonate and 450 were matched. (nih.gov)
- In the North-American dataset, of the 23 711 included patients, 4902 (20.6%) received sodium bicarbonate and 1238 were matched. (nih.gov)
- CONCLUSION: In patients with OHCA, prehospital sodium bicarbonate administration was not associated with neurologic outcomes in a French dataset and was associated with worse neurologic outcomes in a North-American dataset. (nih.gov)
- undertaken from July 15th, 2017 to March 15th, 2018.The multicentrique de cohorte prospective a inclus des Glasgow Coma Scale helped to determine the severety of the patients consécutifs admis en phase aiguë d AVC, disease at admission. (who.int)
- More than half of critically des patients avec AVC en phase aiguë présentent ill patients exhibit admission hyperglycemia with age, severity of stroke and known diabetes as its main associated principaux facteurs de risque a risk factors. (who.int)
- Sodium bicarbonate is an antacid used to relieve heartburn and acid indigestion. (medlineplus.gov)
- This investigation should provide needed information on the appropriate dosing regimen and on the study population that should be enrolled in a future long-term bicarbonate intervention trial to assess the long-term effects of this simple, low cost intervention on important clinical outcomes including rates of loss in bone and muscle mass, falls, and fractures. (nih.gov)
- Given the considerable variability in sodium bicarbonate use by different prehospital care systems and the potential resuscitation-time bias in the present study, a large randomised clinical trial targeting specific patient subgroups may be needed to determine whether sodium bicarbonate has a role in the prehospital management of prolonged OHCA. (nih.gov)
- We extrapolate that lowering bicarbonate targets in other clinical scenarios like liver failure, pregnancy, and cardiac failure may be prudent and will lead to a lower sodium load. (nih.gov)
- The Journal of Strength and Conditioning Research published a research study examining the effects of creatine, placebo maltodextrin, and creatine + sodium bicarbonate. (stack.com)
- Pre-Wingate bicarbonate concentrations were significantly higher in creatine + sodium bicarbonate (10%), compared with in placebo and creatine, and mean concentrations remained higher after sprint 6. (stack.com)
- INTERVENTION: We investigated whether prehospital bicarbonate administration was associated with better neurologic outcomes. (nih.gov)
- Before proceeding to a long-term bicarbonate intervention study, however, it is important to identify the dose of bicarbonate most likely to be optimal and to characterize the subjects who benefit most from it. (nih.gov)
- Bicarbonate (HCO 3 ¯ ) is a normal constituent of body fluids and the normal plasma level ranges from 24 to 31 mEq/liter. (nih.gov)
- If your doctor has told you to take sodium bicarbonate on a certain schedule, take the missed dose as soon as you remember it. (medlineplus.gov)
- However, no rigorous studies have compared tromethamine and bicarbonate, so the effect on patient outcome is unclear. (medscape.com)
- If you are using sodium bicarbonate as an antacid, it should be taken 1 to 2 hours after meals, with a full glass of water. (medlineplus.gov)
- sodium bicarbonate iv , aspirin-dipyridamole oral Mechanism: affects how the kidney reabsorbs the drug in an nonacidic environment. (rxlist.com)
- Our aim was to study the involvement of intestinal and central nervous melatonin in the neurohumoral control of the duodenal mucosa-protective bicarbonate secretion. (jci.org)
- The price of raw materials, particularly Soda Ash, is predicted to rise in April 2023, which would have a further positive impact on the global Sodium Bicarbonate market. (chemanalyst.com)
- Working in anesthetized rats, we cannulated a 12-mm segment of duodenum with an intact blood supply and titrated the local bicarbonate secretion with pH-stat. (jci.org)
- The sodium bicarbonate cotransporter (NBCe1) is essential for normal development of mouse dentition. (bvsalud.org)
- Be the first to review Sodium bicarbonate and earn rewards! (rndsystems.com)
- Ryan International is one of the highly recognized Soda Ash Suppliers in , offering bulk quantity of Sodium Bicarbonate to different industries. (ryan-international.in)
- These and other data support a potential role for bicarbonate as a means of reducing the musculoskeletal declines that lead to extensive morbidity and mortality in the elderly. (nih.gov)
- If sodium bicarbonate does not improve your symptoms, call your doctor. (medlineplus.gov)
- Creatine did make a marked difference, but results from creatine + sodium bicarbonate were significant. (stack.com)
- With the commencement of the upcoming month, Sodium Bicarbonate prices are likely to increase. (chemanalyst.com)