Dopamine

153.18

153.18

200-110-0

VTD58H1Z2X

173182

DTXSID6022420

C62025

Stout prisms

C - Cardiovascular system

66.5

-0.98

Solid

1.2±0.1 g/cm3

128 °C

227 °C

158.0±23.7 °C

1.619

H2O: 535 mg/mL

Some commercially available injections of dopamine in dextrose provided in plastic containers should be stored at room temperature (25 deg C), although brief exposure to temperatures up to 40 deg C does not adversely affect the injections; the injections should be protected from excessive heat and should not be frozen..

1.6X10-5 mm Hg at 25 deg C (est)

Abdominal cavity-rat LD50: 163 mg/kg; abdominal cavity-mouse LD50: 950 mg/kg

Flammable, decomposes toxic nitrogen oxide gas when burning

8.93None

Henry's Law constant = 8.8X10-15 atm-cu m/mol at 25 °C (est)

8.93|pKa = 8.93 (conjugate acid)|pKa1 = 8.71 (phenol); pKa2 = 10.90 (amine); pKa3 = 13.68 (phenol) (est)

129.51 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|125.24 Ų [M+H]+ [CCS Type: DT, Method: stepped-field]|135.36 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|142.3 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|131.8 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|127.7 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]|133.3 Ų [M-H]-

Free base; highly sensitive to oxygen; discolors quickly|Rosettes of needles from water; decomp at 241 °C; may be recrystallized from methanol + ether /Hydrochloride/|Crystals; decomp at 210-214 °C /Hydrobromide/|WHITE CRYSTALLINE POWDER /HYDROCHLORIDE/|For more Other Experimental Properties (Complete) data for DOPAMINE (6 total), please visit the HSDB record page.

UX1092000

Warehouse low temperature, ventilated, dry

Extremely unstable in alkaline media; sensitive to light; stable for 1 yr at 55 deg C /Hydrochloride/

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl dopamine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Dopamine hydrochloride/

Wear approved respiratory protection, chemically compatible gloves and protective clothing. /Dopamine hydrochloride/

This material is assumed to be combustible. /Dopamine hydrochloride/

Water spray, dry chemical, carbon dioxide or foam as appropriate for surrounding fire and materials. This material is assumed to be combustible. As with all dry powders it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity. As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing. /Dopamine hydrochloride/

Wipe up spillage or collect spillage using a high efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately-labelled container for disposal. Wash spill site. /Dopamine hydrochloride/

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Possible eye, skin, ... and/or respiratory tract irritation. /Dopamine hydrochloride/

moderately toxic

LD50 oral mice = 1460 mg/kg, LD50 oral rats = 1780 mg/kg. Spasm or closing of eyelids, nausea, vomiting, cardiac arrhythmias, involuntary movements of the body including the face, tongue, arms, hand, head, and upper body; hypotension, haemolytic anaemia, urinary retention, duodenal ulcer, sialorrhea, ataxia, abdominal pain, dry mouth, nightmares, tachypnoea, bruxism, confusion, and insomnia.

Monoamine oxidase inhibition by furazolidone ... exposes pt to hazards of potential hypertensive crisis if ... other amine-releasing agents /dopamine/ are taken concurrently.|... Possibility of enhanced pharmacological response to phenylephrine and other predominantly direct-acting alpha-adrenergic sympathomimetic amines (eg, dopamine ...) in pt who are receiving or have recently received guanethidine.|Effects on brain dopamine metab in rats studied ; chlorpromazine, thioridazine, and thiethylperazine produced dose-dependent incr in brain concn of 3,4-dihydroxyphenylacetic acid, which were correlated with antipsychotic efficacy.|... Administration of deprenyl inhibits the intracerebral metabolic degradation of dopamine.|For more Interactions (Complete) data for DOPAMINE (12 total), please visit the HSDB record page.

LD50 Rat ip 163 mg/kg|LD50 Mouse ip 950 mg/kg|LD50 Mouse iv 59 mg/kg|LD50 Mouse intracervical 74 mg/kg|LD50 Dog iv 79 mg/kg

Dopamine should be used with caution in patients with ischemic heart disease. The drug is contraindicated in patients with pheochromocytoma and in patients with uncorrected tachyarrhythmias or ventricular fibrillation.

No information currently available on protein binding.

Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylamine.

NIOSH (NOES Survey 1981-1983) has statistically estimated that 8,422 workers (7,695 of these were female) were potentially exposed to dopamine in the US(1).

For the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure|Treatment of vascular hypotensive disorders

Cardiotonic Agents|Dopamine also is used to increase cardiac output and blood pressure in advanced cardiovascular life support (ACLS) during cardiopulmonary resuscitation. Dopamine may be considered in the treatment of symptomatic bradycardia unresponsive to atropine, as a temporizing measure while awaiting availability of a pacemaker, or if pacing is ineffective. During resuscitation, dopamine therapy often is used for the management of hypotension, particularly if associated with symptomatic bradycardia or after return of spontaneous circulation. Dopamine combined with other agents, such as dobutamine, also may be a useful option in the management of postresuscitation hypotension. If hypotension persists after filling pressure (i.e., intravascular volume) is optimized, drugs with combined inotropic and vasopressor actions (e.g., epinephrine, norepinephrine) may be used. Some evidence from animal studies suggests that epinephrine may be more effective than dopamine in improving hemodynamics during cardiopulmonary resuscitation. In addition, epinephrine generally is preferred for patients with severe bradycardia and associated hypotension since pulseless electrical activity or even asystole may be imminent. /Included in US product label/|The net hemodynamic effects of dopamine make it particularly useful in the treatment of cardiogenic shock (including that associated with acute myocardial infarction) or in shock in which oliguria is refractory to other vasopressor agents. Some experts state that dopamine may be considered for the treatment of drug-induced hypovolemic shock, and often is the recommended initial agent for this use when the patient is unresponsive to fluid volume expansion and inotropic and/or vasopressor support is required. The drug can be used as an adjunct (to increase cardiac output further and maintain blood pressure) to afterload reduction with vasodilators (e.g., sodium nitroprusside) in patients with left ventricular failure following acute myocardial infarction when arterial pressure decreases precipitously during afterload reduction; for less precipitous decreases, dobutamine may be preferred but should not be used alone in severely hypotensive patients. In patients with hypotensive cardiogenic shock following acute myocardial infarction, dopamine may be used to replace norepinephrine therapy once systemic arterial pressure has increased to at least 80 mm Hg. Once arterial blood pressure has been stabilized to at least 90 mm Hg, dobutamine may be used concomitantly with dopamine in such patients in an attempt to reduce dopamine requirements. Dopamine also has been used to support cardiac output and maintain arterial pressure during intra-aortic balloon counterpulsation therapy (e.g., in patients with hypotensive cardiogenic shock following acute myocardial infarction). The use of dopamine in low cardiac output syndrome following open heart surgery has been shown to increase long-term survival. However, because dobutamine lowers peripheral resistance over a wide dosage range, is not dependent on release of endogenous catecholamines for its effects, and is cardioselective, that drug may be preferable in the period immediately following cardiopulmonary bypass surgery. /Included in US product label/|Dopamine is used to increase cardiac output, blood pressure, and urine flow as an adjunct in the treatment of shock that persists after adequate fluid volume replacement and when systemic vascular resistance is decreased. /Included in US product label/|For more Therapeutic Uses (Complete) data for DOPAMINE (12 total), please visit the HSDB record page.

Dopamine should be used with caution in patients with ischemic heart disease. The drug is contraindicated in patients with pheochromocytoma and in patients with uncorrected tachyarrhythmias or ventricular fibrillation.|Commercially available formulations of dopamine hydrochloride may contain sulfites that can cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals. The overall prevalence of sulfite sensitivity in the general population is unknown but probably low; such sensitivity appears to occur more frequently in asthmatic than in nonasthmatic individuals.|Caution should be used to avoid extravasation of the drug. Dopamine should be administered through a long IV catheter into a large vein, preferably in the antecubital fossa rather than the hand or ankle. One manufacturer states that administration into an umbilical arterial catheter is not recommended. If larger veins are unavailable and the condition of the patient requires that the hand or ankle veins be used to administer dopamine, the injection site should be changed to a larger vein as soon as possible. The injection site should be carefully monitored.|Patients with a history of occlusive vascular disease (e.g., atherosclerosis, arterial embolism, Raynaud's disease, cold injury, diabetic endarteritis, or Buerger's disease) should be carefully monitored during dopamine therapy for decreased circulation to the extremities indicated by changes in color or temperature of the skin or pain in the extremities. If these occur, they may be corrected by decreasing the rate of infusion or discontinuing dopamine; however, these changes occasionally have persisted and progressed after discontinuing dopamine. The potential benefits of continuing dopamine should be weighed against the possible risk of necrosis.|For more Drug Warnings (Complete) data for DOPAMINE (13 total), please visit the HSDB record page.

Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings.

Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons. (See all compounds classified as Dopamine Agents.)|Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters. (See all compounds classified as Sympathomimetics.)|Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)

Dopamine is rapidly absorbed from the small intestine.|It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged.|Dopamine is frequently used in critically ill newborn infants for treatment of shock and cardiac failure, but its pharmacokinetics has not been evaluated using a specific analytical method. Steady-state arterial plasma concentrations of dopamine were measured in 11 seriously ill infants receiving dopamine infusion, 5-20 ug/kg-1.min-1, for presumed or proven sepsis and hypotensive shock. Steady-state concentrations of dopamine ranged from 0.013-0.3 ug/mL. Total body clearance averaged 115 mL/kg-1.min-1. The apparent volume of distribution and elimination half life averaged 1.8 l.kg-1 and 6.9 min, respectively. No relationship was observed between dopamine pharmacokinetics and gestational age, postnatal age or birthweight. Substantial interindividual variation was seen in dopamine pharmacokinetics in seriously ill infants, and plasma concentrations could not be predicted accurately from its infusion rate. Marked variation in clearance explains in part, the wide dose requirements of dopamine needed to elicit clinical response in critically ill newborn infants.|Less than 10% of a dose is recovered unchanged in the urine.|Plasma dopamine concentrations /of children (age 3 months to 13 yrs) recovering from cardiac surgery or shock/ were measured at the steady state or at termination of infusion using high-performance liquid chromatography. The half-lives of distribution and elimination were 1.8 +/- 1.1 and 26 +/- 14 (SD) mins, respectively. The apparent volume of distribution was 2952 +/- 2332 mL/kg. The clearance rate was 454 +/- 900 mL/kg.min. Dopamine clearance was linearly related to dose only in patients who were also receiving dobutamine (r2 = .76, p less than .05). Hepatic and renal dysfunction did not affect the pharmacokinetics of dopamine. A relationship between dopamine and dobutamine that affects the disposition of these two drugs may exist. The pharmacokinetics of dopamine are variable even in hemodynamically stable children. Hepatic or renal function does not adversely affect the pharmacokinetics of dopamine.|The brain contains separate neuronal systems that utilize 3 different catecholamines- dopamine, norepinephrine, and epinephrine ... More than half of the central nervous system content of catecholamine is dopamine and extremely high amt are found in the basal ganglia (especially the caudate nucleus), the nucleus accumbens, the olfactory tubercle, the central nucleus of the amygdala, the median eminence, and restricted fields of the frontal cortex.|Dopamine is widely distributed in the body but does not cross the blood-brain barrier to a substantial extent. The apparent volume of distribution of the drug in neonates ranges from 0.6-4 L/kg. It is not known if dopamine crosses the placenta.

Biotransformation of dopamine proceeds rapidly to yield the principal excretion products, 3-4-dihydroxy-phenylacetic acid (DOPAC) and 3-methoxy-4-hydroxy-phenylacetic acid (homovanillic acid, HVA).|Dopamine is extensively metabolized in the liver. ... Hepatic metabolism results in inactive metabolites (75% of the dose) and norepinephrine (active, 25% of the dose) in the adrenergic nerve terminals. The principal means of elimination appear to be O-methylation by catechol-O-methyltransferase to form 3-methoxytyramine, followed either by sulfoconjugation (by phenosulfotransferase) or by deamination (by monoamine oxidase (MAO)) to homovanillic acid. Approximately 80% of the drug is excreted in the urine as homovanillic acid, homovanillic acid metabolites, and norepinephrine metabolites within 24 hours.|Yields N-acetyl-3,4-dihydroxyphenethylamine in man, in rat; Hauson A, Studnitz W Von; Clinica Chim Acta 11: 384 (1965); Goldstein M, Musacchio Jm; Biochim Biophys Acta 58: 607 (1962). Yields 3,4-dihydroxy-n-methylphenethylamine in rat; Laduron P; Nature New Biology 238: 212 (1972). /From table/|Yields 3,4-dihydroxyphenethylamine-o-beta-d-glucuronide in rat; Young Ja, Edwards Kdg; J Pharmac Exp Ther 145: 102 (1964). Yields 3,4-dihydroxyphenylacetaldehyde in man and rat; Nagatsu T et al; Enzymologia 39: 15 (1970); Goldstein M et al; Biochim Biophys Acta 33: 572 (1959). /From table/|Yields 4-hydroxyphenethyamin-3-yl sulfate in rat; Jenner Wn, Rose Fa; Biochem J 135: 109 (1973). Yields 3-methoxytyramine in man; Goodall MCC, Alton A; Biochem Pharmac 17: 905 (1968). Yields d-noradrenaline in man; Sjoerdsma AJ et al; J Clin Invest 38: 31 (1959). /From table/|For more Metabolism/Metabolites (Complete) data for DOPAMINE (8 total), please visit the HSDB record page.|Dopamine has known human metabolites that include Dopamine 4- D-Glucuronide and dopamine 3-O-sulfate.

2 minutes|Plasma dopamine concentrations /of children (age 3 months to 13 yrs) recovering from cardiac surgery or shock/ were measured at the steady state or at termination of infusion using high-performance liquid chromatography. The half-lives of distribution and elimination were 1.8 +/- 1.1 and 26 +/- 14 (SD) mins, respectively.|Dopamine has a plasma half-life of about 2 minutes. In neonates, the elimination half-life of dopamine reportedly is 5-11 minutes.

Dopamine is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings. In the brain, dopamine actas as an agonist to the five dopamine receptor subtypes (D!, D2, D3, D4, D5).|Dopamine acts on cardiac beta-1-adrenergic receptors and has dosage-dependent effects on peripheral receptors. Dopamine receptors are activated at a low infusion rate (0.5-2 ug/kg/min). At a rate > 4-6 ug/kg/min, peripheral alpha-adrenergic receptors are activated, and vasoconstriction and increased afterload may occur.|The effects that dopamine produces in the body are directly related to its actions on alpha, beta, and dopaminergic receptor sites. When these receptors are stimulated cyclic adenosine monophosphate levels increase, increasing calcium transport into the cell. The amount of dopamine determines which receptors are predominantly stimulated. At infusion rates more than 5 to 10 ug/kg/minute, alpha-receptor stimulation predominates, resulting in peripheral vasoconstriction, with a rise in blood pressure. At infusion rates greater than 20 ug/kg/minute, the vasoconstrictive effect can be greater than the beta1 effect.|The cardiovascular effects of dopamine are mediated by several distinct types of receptors that vary in their affinity for dopamine. At low concentrations, the primary interaction of dopamine is with vascular D1 receptors, especially in the renal, mesenteric, and coronary beds. By activating adenylyl cyclase and raising intracellular concentrations of cyclic AMP, D1 receptor stimulation leads to vasodilation. Infusion of low doses of dopamine causes an increase in glomerular filtration rate, renal blood flow, and Na+ excretion. Activation of D1 receptors on renal tubular cells decreases sodium transport by cAMP-dependent and cAMP-independent mechanisms. Increasing cAMP production in the proximal tubular cells and the medullary part of the thick ascending limb of the loop of Henle inhibits the Na+-H+ exchanger and the Na+,K+-ATPase pump. The renal tubular actions of dopamine that cause natriuresis may be augmented by the increase in renal blood flow and the small increase in the glomerular filtration rate that follow its administration. The resulting increase in hydrostatic pressure in the peritubular capillaries and reduction in oncotic pressure may contribute to diminished reabsorption of sodium by the proximal tubular cells.|At somewhat higher concentrations, dopamine exerts a positive inotropic effect on the myocardium, acting on beta1 adrenergic receptors. Dopamine also causes the release of norepinephrine from nerve terminals, which contributes to its effects on the heart. Tachycardia is less prominent during infusion of dopamine than of isoproterenol. Dopamine usually increases systolic blood pressure and pulse pressure and either has no effect on diastolic blood pressure or increases it slightly. Total peripheral resistance usually is unchanged when low or intermediate doses of dopamine are given, probably because of the ability of dopamine to reduce regional arterial resistance in some vascular beds, such as mesenteric and renal, while causing only minor increases in others. At high concentrations, dopamine activates vascular alpha1 receptors, leading to more general vasoconstriction.|For more Mechanism of Action (Complete) data for DOPAMINE (9 total), please visit the HSDB record page.

4-O-methyldopamine

Remove from exposure. Remove contaminated clothing. Persons developing serious hypersensitivity (anaphylactic) reactions must receive immediate medical attention. If person is not breathing give artificial respiration. If breathing is difficult give oxygen. Obtain medical attention. /Dopamine hydrochloride/|In the event of an overdose, supportive and symptomatic measures should be used. If blood pressure fails to lower, a short-acting alpha adrenergic blocking agent, such as phentolamine, may be administered. /Dopamine hydrochloride/|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Possible allergic reaction to material if inhaled, ingested, or in contact with skin. /Dopamine hydrochloride/|/SIGNS AND SYMPTOMS/ Overdose effects include severe increase in blood pressure. /Dopamine hydrochloride/|/SIGNS AND SYMPTOMS/ Extravasation of large amt of dopamine into local tissue may cause ischemic necrosis and slough. Gangrene of fingers and toes after prolonged infusion has been reported.|/SIGNS AND SYMPTOMS/ Ventricular arrhythmias and hypertension may occur when usual doses of dopamine are administered during halothane (or other halogenated hydrocarbon) or cyclopropane anesthesia. Extreme caution should be used when administering dopamine to patients receiving these general anesthetics which increase cardiac irritability. Results of studies in animals indicate that dopamine-induced ventricular arrhythmias during anesthesia can be reversed by propranolol.|For more Human Toxicity Excerpts (Complete) data for DOPAMINE (12 total), please visit the HSDB record page.

3,4 Dihydroxyphenethylamine

Table: Dopamine Hydrochloride Preparations [Table#4381]|Table: Dopamine Hydrochloride in Dextrose Preparations [Table#4382]

One of the catecholamine neurotransmitters in the brain. ... important in regulating movement|The compatability of dopamine hydrochloride with various additives in 5% dextrose injection USP was established.

Analyte: dopamine hydrochloride; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /Dopamine hydrochloride/|Analyte: dopamine hydrochloride; matrix: chemical identification; procedure: ultraviolet absorption spectrophotometry with comparison to standards /Dopamine hydrochloride/|Analyte: dopamine hydrochloride; matrix: chemical purity; procedure: dissolution in formic acid; addition of acetic anhydride; potentiometric titration with perchloric acid /Dopamine hydrochloride/|For more Analytic Laboratory Methods (Complete) data for DOPAMINE (11 total), please visit the HSDB record page.

Analyte: dopamine hydrochloride; matrix: pharmaceutical preparation (injection solution); procedure: thin-layer chromatography with comparison to standards (chemical identification) /Dopamine hydrochloride/|Analyte: dopamine hydrochloride; matrix: pharmaceutical preparation (injection solution); procedure: liquid chromatography with ultraviolet detection at 280 nm and comparison to standards (chemical purity) /Dopamine hydrochloride/|Analyte: dopamine; matrix: urine; procedure: high-performance liquid chromatography with electrochemical detection; limit of detection: 3 ng/mL|Analyte: dopamine; matrix: blood (plasma); procedure: high-performance liquid chromatography with electrochemical detection and fluorescence detection at 350 nm (excitation) and 480 nm (emission); limit of detection: 3 pg/mL|For more Clinical Laboratory Methods (Complete) data for DOPAMINE (11 total), please visit the HSDB record page.

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