Sodium bicarbonate   中文名称: 碳酸氢钠

对于生命科学相关的研究，碳酸钠（99.5%）是一种生化试剂，可用作有机物质或生物材料。

Absorption, Distribution and Excretion
Elimination: Renal; carbon dioxide formed is eliminated via lungs.
Excess sodium bicarbonate is emptied rapidly into small intestine where it is absorbed.
It is eliminated principally in the urine and effectively alkalizes it. ... /It/ is completely absorbed orally and usually is excreted within 3-4 hr.
Oral: Onset of action: Rapid; Duration: 8-10 minutes. I.V: Onset of action: 15 minutes; duration: 1-2 hours.
For more Absorption, Distribution and Excretion (Complete) data for Sodium bicarbonate (8 total), please visit the HSDB record page.

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Metabolism / Metabolites
Excessive use can cause systemic alkalosis /in animals/, but body usually splits bicarbonate radical into water and carbon dioxide ...
Sodium bicarbonate rapidly reacts with hydrochloric acid to form sodium chloride, carbon dioxide, and water; excess bicarbonate that does not neutralize gastric acid rapidly empties into the small intestine and is absorbed.

Toxicity Summary
IDENTIFICATION AND USE: Sodium bicarbonate is a white crystalline powder or granules. It is used in manufacturing many sodium salts, as a source of carbon dioxide, ingredient of baking powder, and effervescent salts and beverages, in fire extinguishers, cleaning compounds. It is also used in analytical chemistry for pH adjustment. It is used in aquaculture as an anesthetic for fish in the United States. Sodium bicarbonate is used in the treatment of metabolic acidosis associated with many conditions. It is also used in veterinary medicine. HUMAN STUDIES: Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The anticoagulant effects of sodium bicarbonate was investigated in fresh human whole blood obtained from normal healthy volunteers. Prothrombin and thrombin clotting time determination indicated that bicarbonate can interfere with the clotting process. ANIMAL STUDIES: Sodium bicarbonate was irritating to the rabbit eye. It was slightly irritating when tested on the skin of rabbits. Sodium bicarbonate was evaluated for teratological effects, maximum dose levels were as follows: mice, 580 mg/kg; rats, 340 mg/kg; and rabbits, 330 mg/kg. No effects were found in any of these species. The mutagenicity of sodium bicarbonate was assessed in Salmonella/microsome assays using Salmonella typhimurium strains TA 92, TA 94, TA 98, TA 100, TA 1535 and TA 1537 with metabolic activation, and it was negative. ECOTOXICITY STUDIES: Several histological anomalies, including increased incidence of necrotic cells, suggested that fish were adversely affected as a result of exposure to >450 mg NaHCO3/L.

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Toxicity Data
LC (rat) = > 900 mg/m3

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Interactions
Concurrent use /of citrates/ with sodium bicarbonate may promote the development of calcium stones in patients with uric acid stones, due to sodium ion opposition to the hypocalciuric effect of the alkaline load; may also cause hypernatremia.
Chronic administration of bicarbonate with milk or calcium may cause the milk-alkali syndrome which is characterized by hypercalcemia, renal insufficiency, metabolic alkalosis, nausea, vomiting, headache, mental confusion, and anorexia. During the acute phase of the milk-alkali syndrome, the condition is reversible when the calcium and alkali are withdrawn. However, in patients with chronic milk-alkali syndrome, reduced renal function may persist even after calcium and alkali are discontinued. Patients with a salt-losing nephropathy have an increased risk of developing the milk-alkali syndrome.
Concurrent use /of anticholinergics or other medications with anticholinergic action/ with sodium bicarbonate may decrease absorption, reducing the effectiveness of the anticholinergic; doses of these medications should be spaced 1 hour apart from doses of sodium bicarbonate; also, urinary excretion may be delayed by alkalinization of the urine, thus potentiating the side effects of the anticholinergic
Antacids may alkalinize the urine and counteract the effect of urinary acidifiers /such as ammonium chloride, ascorbic acid and potassium or sodium phosphates/; frequent use of antacids, especially in high doses, is best avoided by patients receiving therapy to acidify the urine.
For more Interactions (Complete) data for Sodium bicarbonate (17 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat oral 4,220 mg/kg
LD50 Mouse oral 3360 mg/kg

Sodium bicarbonate appears as odorless white crystalline powder or lumps. Slightly alkaline (bitter) taste. pH (of freshly prepared 0.1 molar aqueous solution): 8.3 at 77 °F. pH (of saturated solution): 8-9. Non-toxic.
Sodium hydrogencarbonate is an organic sodium salt and a one-carbon compound. It has a role as an antacid and a food anticaking agent. It contains a hydrogencarbonate.
Sodium bicarbonate is a white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.
Sodium Bicarbonate is the monosodium salt of carbonic acid with alkalinizing and electrolyte replacement properties. Upon dissociation, sodium bicarbonate forms sodium and bicarbonate ions. Ion formation increases plasma bicarbonate and buffers excess hydrogen ion concentration, resulting in raised blood pH.
Soda is a beverage consisting of carbonated water and a flavoring.
A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.
See also: Bicarbonate Ion (has active moiety); Sodium Cation (has active moiety); Omeprazole; Sodium Bicarbonate (component of) ... View More ...

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Drug Indication
Sodium bicarbonate is used for 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. Also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturateprotein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of blood pigments.

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Mechanism of Action
Sodium bicarbonate is a systemic alkalizer, which increases plasma bicarbonate, buffers excess hydrogen ion concentration, and raises blood pH, thereby reversing the clinical manifestations of acidosis. It is also a urinary alkalizer, increasing the excretion of free bicarbonate ions in the urine, thus effectively raising the urinary pH. By maintaining an alkaline urine, the actual dissolution of uric acid stones may be accomplished. Sodium bicarbonate acts as an antacid and reacts chemically to neutralize or buffer existing quantities of stomach acid but has no direct effect on its output. This action results in increased pH value of stomach contents, thus providing relief of hyperacidity symptoms. [PharmGKB]

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Therapeutic Uses
Sodium bicarbonate is used in the treatment of metabolic acidosis associated with many conditions including severe renal disease (e.g., renal tubular acidosis), uncontrolled diabetes (ketoacidosis), extracorporeal circulation of the blood, cardiac arrest, circulatory insufficiency caused by shock or severe dehydration, ureterosigmoidostomy, lactic acidosis, alcoholic ketoacidosis, use of carbonic anhydrase inhibitors, and ammonium chloride administration. In metabolic acidosis, the principal disturbance is a loss of proton acceptors (e.g., loss of bicarbonate during severe diarrhea) or accumulation of an acid load (e.g., ketoacidosis, lactic acidosis, renal tubular acidosis).
The specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis has not been established. Because correction of the underlying metabolic disorder generally results in correction of acid-base abnormalities and because of the potential risks of sodium bicarbonate therapy in the treatment of this disorder, administration of sodium bicarbonate is generally reserved for the treatment of severe acidosis (e.g., arterial pH less than 7-7.15 or serum bicarbonate concentration of 8 mEq/L or less). Rapid correction of acidosis with sodium bicarbonate in patients with diabetic ketoacidosis may cause hypokalemia, paradoxical acidosis in cerebrospinal fluid (CSF) since carbon dioxide diffuses more rapidly into CSF than does bicarbonate, and lactic acidosis since increased pH increases hemoglobin-oxygen affinity which, when combined with erythrocyte 2,3-diphosphoglycerate (2,3-DPG) deficiency in these patients, results in peripheral tissue hypoxia. However, the benefits and risks of sodium bicarbonate therapy in ketoacidosis have not been fully determined, and additional controlled studies of the safety and efficacy of the drug are necessary. Generally, when sodium bicarbonate is used in the treatment of diabetic ketoacidosis, the acidosis should only be partially corrected (e.g., to an arterial pH of about 7.2) to avoid rebound metabolic alkalosis as ketones are metabolized.
Oral sodium bicarbonate is indicated to reduce uric acid crystallization as an adjuvant to uricosuric medication in gout. /Included in US product labeling/
Parenteral sodium bicarbonate is indicated in the treatment of certain drug intoxications, including barbiturates, and in poisoning by salicylates or methyl alcohol. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for Sodium bicarbonate (29 total), please visit the HSDB record page.

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Drug Warnings
Sodium bicarbonate is generally contraindicated in patients with metabolic or respiratory alkalosis, in patients with hypocalcemia in whom alkalosis may induce tetany, in patients with excessive chloride loss from vomiting or continuous GI suctioning, and in patients at risk of developing diuretic-induced hypochloremic alkalosis. Sodium bicarbonate should not be used orally as an antidote in the treatment of acute ingestion of strong mineral acids, since carbon dioxide gas forms during neutralization and may cause gastric distention and possible rupture.
Sodium bicarbonate should be used with extreme caution in patients with congestive heart failure or other edematous or sodium-retaining conditions; in patients with renal insufficiency, especially those with severe insufficiency such as oliguria or anuria; and in patients receiving corticosteroids or corticotropin, since each gram of sodium bicarbonate contains about 12 mEq of sodium. IV administration of sodium bicarbonate may cause fluid and/or solute overload resulting in dilution of serum electrolytes, overhydration, congestive conditions, or pulmonary edema. The risk of dilutional conditions is inversely proportional to the electrolyte concentration administered, and the risk of solute overload and resultant congestive conditions with peripheral and/or pulmonary edema is directly proportional to the electrolyte concentration administered.
Gastric distention and flatulence may occur when sodium bicarbonate is administered orally. Inadvertent extravasation of hypertonic solutions of sodium bicarbonate has reportedly caused chemical cellulitis because of their alkalinity, subsequently resulting in tissue necrosis, ulceration, and/or sloughing at the site of injection.
Predisposing factors /contributing to milk-alkali syndrome/ are preexisting hypertension, sarcoidosis, dehydration and electrolyte imbalance due to vomiting or aspiration of gastric contents with inadequate iv fluid replacement, and renal dysfunction caused by primary renal disease.
For more Drug Warnings (Complete) data for Sodium bicarbonate (14 total), please visit the HSDB record page.

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Pharmacodynamics
Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis.

CHNAO3

84.0

83.982

144-55-8

7542-12-3 (unspecified hydrochloride salt)

516892

White to off-white solid powder

2.16 g/mL at 25 °C(lit.)

851°C

270 ºC

169.8ºC

2.58E-05mmHg at 25°C

1.500

60.36

1

3

0

5

33.9

0

UIIMBOGNXHQVGW-UHFFFAOYSA-M

InChI=1S/CH2O3.Na/c2-1(3)4;/h(H2,2,3,4);/q;+1/p-1

sodium;hydrogen carbonate

Soda Mint Sodium hydrocarbonateSodium bicarbonate NSC-134031 NSC 134031 NSC134031Bicarbonate of soda

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~50 mg/mL (~595.17 mM)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。