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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/24 10:16:45」(JST)

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Epinephrine, also known as adrenalin or adrenaline, is primarily a medication and hormone.^[3]^[4] As a medication it is used for a number of conditions including: anaphylaxis, cardiac arrest, and superficial bleeding.^[1] Inhaled epinephrine may be used to improve the symptoms of croup.^[5] It may also be used for asthma when other treatments are not effective. It is given intravenously, by injection into a muscle, by inhalation, or by injection just under the skin.^[1]

Common side effects include shakiness, anxiety, and sweating. A fast heart rate and high blood pressure may occur. Occasionally it may result in an abnormal heart rhythm. While the safety of its use during pregnancy and breastfeeding is unclear, the benefits to the mother must be taken into account.^[1]

Epinephrine is normally produced by both the adrenal glands and certain neurons.^[3] It plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar.^[6]^[7] Epinephrine does this by its effects on alpha and beta receptors.^[7] It is found in many animals and some one cell organisms.^[8]^[9]

Jokichi Takamine first isolated epinephrine in 1901.^[10] It is on the World Health Organization's List of Essential Medicines, the most important medication needed in a basic health system.^[11] It is available as a generic medication.^[1] The wholesale cost is between 0.10 and 0.95 USD a vial.^[12] An autoinjector, as of 2015, costs about 100 USD and is available for use in anaphylaxis.^[1]

1 Medical uses
- 1.1 Cardiac arrest
- 1.2 Anaphylaxis
- 1.3 Asthma
- 1.4 Croup
- 1.5 Local anesthetics
2 Adverse effects
3 Physiology effects
- 3.1 Exercise
- 3.2 Emotional response
- 3.3 Memory
4 Pathology
5 Terminology
6 Mechanism of action
7 Measurement in biological fluids
8 Biosynthesis and regulation
- 8.1 Regulation
9 History
10 Society and culture
- 10.1 Names
- 10.2 Strength
11 References
12 General references
13 External links

Medical uses

Epinephrine vial 1 mg (Adrenalin)

Epinephrine is used to treat a number of conditions including: cardiac arrest, anaphylaxis, and superficial bleeding.^[13] It has been used historically for bronchospasm and hypoglycemia, but newer treatments for these that are selective for β₂ adrenoceptors, such as salbutamol are currently preferred.

Cardiac arrest

While epinephrine is often used to treat cardiac arrest it has not been shown to improve long-term survival or improve mental function after recovery.^[14]^[15] It does, however, improve return of spontaneous circulation.^[15]

Anaphylaxis

Epinephrine is the drug of choice for treating anaphylaxis. Different strengths, doses and routes of administration of epinephrine are used.

The commonly used epinephrine autoinjector delivers a 0.3 mg epinephrine injection (0.3 mL, 1:1000) and is indicated in the emergency treatment of allergic reactions including anaphylaxis to stings, contrast agents, medicines or people with a history of anaphylactic reactions to known triggers. A single dose is recommended for people who weigh 30 kg or more, repeated if necessary. A lower strength product is available for children.^[16]^[17]^[18]^[19]

Intramuscular injection can be complicated in that the depth of subcutaneous fat varies and may result in subcutaneous injection, or may be injected intravenously in error, or the wrong strength used.^[20] Intramuscular injection does give a faster and higher pharmacokinetic profile when compared to SC injection ^[21]

Asthma

Epinephrine is also used as a bronchodilator for asthma if specific β₂ agonists are unavailable or ineffective.^[22]

When given by the subcutaneous or intramuscular routes for asthma, an appropriate dose is 0.3 to 0.5mg.^[23]^[24]

Croup

Racemic epinephrine has historically been used for the treatment of croup.^[25]^[26] Regular epinephrine however works equally well. Racemic adrenaline is a 1:1 mixture of the dextrorotatory (d) and levorotatory (l) isomers of adrenaline.^[27] The l- form is the active component.^[27] Racemic adrenaline works by stimulation of the α-adrenergic receptors in the airway, with resultant mucosal vasoconstriction and decreased subglottic edema, and by stimulation of the β-adrenergic receptors, with resultant relaxation of the bronchial smooth muscle.^[26]

Local anesthetics

Adrenaline is added to injectable forms of a number of local anesthetics, such as bupivacaine and lidocaine, as a vasoconstrictor to slow the absorption and, therefore, prolong the action of the anesthetic agent. Due to epinephrine's vasoconstricting abilities, the use of epinephrine in localized anesthetics also helps to diminish the total blood loss the patient sustains during minor surgical procedures. Some of the adverse effects of local anesthetic use, such as apprehension, tachycardia, and tremor, may be caused by adrenaline. Epinephrine/adrenalin is frequently combined with dental and spinal anesthetics and can cause panic attacks in susceptible patients at a time when they may be unable to move or speak due to twilight anesthesia.^[28] Currently the maximum recommended daily dosage for people in a dental setting requiring local anesthesia with a peripheral vasoconstrictor is 10 µg/lb of total body weight.^[13]^{[not in citation given]}

Adrenaline is mixed with cocaine to form Moffett's Solution, used in nasal surgery.

Adverse effects

Adverse reactions to adrenaline include palpitations, tachycardia, arrhythmia, anxiety, panic attack, headache, tremor, hypertension, and acute pulmonary edema.^[29]

Use is contraindicated in people on nonselective β-blockers, because severe hypertension and even cerebral hemorrhage may result.^[30] Although commonly believed that administration of adrenaline may cause heart failure by constricting coronary arteries, this is not the case. Coronary arteries have only β₂ receptors, which cause vasodilation in the presence of adrenaline.^[31] Even so, administering high-dose adrenaline has not been definitively proven to improve survival or neurologic outcomes in adult victims of cardiac arrest.^[32]

Physiology effects

The adrenal medulla is a minor contributor to total circulating catecholamines (L-DOPA is at a higher concentration in the plasma),^[33] though it contributes over 90% of circulating epinephrine. Little epinephrine is found in other tissues, mostly in scattered chromaffin cells. Following adrenalectomy, epinephrine disappears below the detection limit in the blood stream.^[34]

The adrenals contribute about 7% of circulating norepinephrine, most of which is a spill over from neurotransmission with little activity as a hormone.^[35]^[36]^[37] Pharmacological doses of epinephrine stimulate α1, α2, β1, β2, and β3 adrenoceptors of the sympathetic nervous system. Sympathetic nerve receptors are classified as adrenergic, based on their responsiveness to adrenaline.^[38]

The term “adrenergic” is often misinterpreted in that the main sympathetic neurotransmitter is norepinephrine (noradrenaline), rather than epinephrine, as discovered by Ulf von Euler in 1946.^[39]^[40]

Epinephrine does have a β2 adrenoceptor mediated effect on metabolism and the airway, there being no direct neural connection from the sympathetic ganglia to the airway.^[41]^[42]^[43]

The concept of the adrenal medulla and the sympathetic nervous system being involved in the flight, fight and fright response was originally proposed by Cannon.^[44] But the adrenal medulla, in contrast to the adrenal cortex, is not required for survival. In adrenalectomized patients haemodynamic and metabolic responses to stimuli such as hypoglycaemia and exercise remain normal.^[45]^[46]

Exercise

One physiological stimulus to epinephrine secretion is exercise. This was first demonstrated using the denervated pupil of a cat as an assay,^[47] later confirmed using a biological assay on urine samples.^[48] Biochemical methods for measuring catecholamines in plasma were published from 1950 onwards.^[49] Although much valuable work has been published using fluorimetric assays to measure total catecholamine concentrations, the method is too non-specific and insensitive to accurately determine the very small quantities of epinephrine in plasma. The development of extraction methods and enzyme-isotope derivate radio-enzymatic assays (REA) transformed the analysis down to a sensitivity of 1 pg for epinephrine.^[50] Early REA plasma assays indicated that epinephrine and total catecholamines rise late in exercise, mostly when anaerobic metabolism commences.^[51]^[52]^[53]

During exercise the epinephrine blood concentration rises partially from increased secretion from the adrenal medulla and partly from decreased metabolism because of reduced hepatic blood flow.^[54] Infusion of epinephrine to reproduce exercise circulating concentrations of epinephrine in subjects at rest has little haemodynamic effect, other than a small β2 mediated fall in diastolic blood pressure.^[55]^[56] Infusion of epinephrine well within the physiological range suppresses human airway hyper-reactivity sufficiently to antagonize the constrictor effects of inhaled histamine.^[57]

A link between what we now know as the sympathetic system and the lung was shown in 1887 when Grossman showed that stimulation of cardiac accelerator nerves reversed muscarine induced airway constriction.^[58] In elegant experiments in the dog, where the sympathetic chain was cut at the level of the diaphragm, Jackson showed that there was no direct sympathetic innervation to the lung, but that bronchoconstriction was reversed by release of epinephrine from the adrenal medulla.^[59] An increased incidence of asthma has not been reported for adrenalectomized patients; those with a predisposition to asthma will have some protection from airway hyper-reactivity from their corticosteroid replacement therapy. Exercise induces progressive airway dilation in normal subjects that correlates with work load and is not prevented by beta blockade.^[60] The progressive dilation of the airway with increasing exercise is mediated by a progressive reduction in resting vagal tone. Beta blockade with propranolol causes a rebound in airway resistance after exercise in normal subjects over the same time course as the bronchoconstriction seen with exercise induced asthma.^[61] The reduction in airway resistance during exercise reduces the work of breathing.^[62]

Emotional response

Every emotional response has a behavioral component, an autonomic component, and a hormonal component. The hormonal component includes the release of epinephrine, an adrenomedullary response that occurs in response to stress and that is controlled by the sympathetic nervous system. The major emotion studied in relation to epinephrine is fear. In an experiment, subjects who were injected with epinephrine expressed more negative and fewer positive facial expressions to fear films compared to a control group. These subjects also reported a more intense fear from the films and greater mean intensity of negative memories than control subjects.^[63] The findings from this study demonstrate that there are learned associations between negative feelings and levels of epinephrine. Overall, the greater amount of epinephrine is positively correlated with an arousal state of negative feelings. These findings can be an effect in part that epinephrine elicits physiological sympathetic responses including an increased heart rate and knee shaking, which can be attributed to the feeling of fear regardless of the actual level of fear elicited from the video. Although studies have found a definite relation between epinephrine and fear, other emotions have not had such results. In the same study, subjects did not express a greater amusement to an amusement film nor greater anger to an anger film.^[63] Similar findings were also supported in a study that involved rodent subjects that either were able or unable to produce epinephrine. Findings support the idea that epinephrine does have a role in facilitating the encoding of emotionally arousing events, contributing to higher levels of arousal due to fear.^[64]

Memory

The biosynthesis of adrenaline involves a series of enzymatic reactions.

It has been found that adrenergic hormones, such as epinephrine, can produce retrograde enhancement of long-term memory in humans. The release of epinephrine due to emotionally stressful events, which is endogenous epinephrine, can modulate memory consolidation of the events, ensuring memory strength that is proportional to memory importance. Post-learning epinephrine activity also interacts with the degree of arousal associated with the initial coding.^[65] There is evidence that suggests epinephrine does have a role in long-term stress adaptation and emotional memory encoding specifically. Epinephrine may also play a role in elevating arousal and fear memory under particular pathological conditions including post-traumatic stress disorder.^[64] Overall, "Extensive evidence indicates that epinephrine (EPI) modulates memory consolidation for emotionally arousing tasks in animals and human subjects.”^[66] Studies have also found that recognition memory involving epinephrine depends on a mechanism that depends on B-adrenoceptors.^[66] Epinephrine does not readily cross the blood–brain barrier, so its effects on memory consolidation are at least partly initiated by B-adrenoceptors in the periphery. Studies have found that sotalol, a B-adrenoceptor antagonist that also does not readily enter the brain, blocks the enhancing effects of peripherally administered epinephrine on memory.^[67] These findings suggest that B-adrenoceptors are necessary for epinephrine to have an effect on memory consolidation.

For noradrenaline to be acted upon by PNMT in the cytosol, it must first be shipped out of granules of the chromaffin cells. This may occur via the catecholamine-H⁺ exchanger VMAT1. VMAT1 is also responsible for transporting newly synthesized adrenaline from the cytosol back into chromaffin granules in preparation for release.^[68]

In liver cells, adrenaline binds to the β-adrenergic receptor, which changes conformation and helps Gs, a G protein, exchange GDP to GTP. This trimeric G protein dissociates to Gs alpha and Gs beta/gamma subunits. Gs alpha binds to adenyl cyclase, thus converting ATP into cyclic AMP. Cyclic AMP binds to the regulatory subunit of protein kinase A: Protein kinase A phosphorylates phosphorylase kinase. Meanwhile, Gs beta/gamma binds to the calcium channel and allows calcium ions to enter the cytoplasm. Calcium ions bind to calmodulin proteins, a protein present in all eukaryotic cells, which then binds to phosphorylase kinase and finishes its activation. Phosphorylase kinase phosphorylates glycogen phosphorylase, which then phosphorylates glycogen and converts it to glucose-6-phosphate.^{[citation needed]}

Pathology

Increased epinephrine secretion is observed in phaeochromocytoma, hypoglycaemia, myocardial infarction and to a lesser degree in benign essential familial tremor. A general increase in sympathetic neural activity is usually accompanied by increased adrenaline secretion, but there is selectivity during hypoxia and hypoglycaemia, when the ratio of adrenaline to noradrenaline is considerably increased.^[69]^[70]^[71] Therefore, there must be some autonomy of the adrenal medulla from the rest of the sympathetic system.

Myocardial infarction is associated with high levels of circulating epinephrine and norepinephrine, particularly in cardiogenic shock.^[72]^[73]

Benign familial tremor (BFT) is responsive to peripheral β-adrenergic blockers and beta 2 stimulation is known to cause tremor. Patients with BFT were found to have increased plasma epinephrine, but not norepinephrine.^[74]^[75]

Low, or absent, concentrations of epinephrine can be seen in autonomic neuropathy or following adrenalectomy. Failure of the adrenal cortex, as with Addisons disease, can suppress epinephrine secretion as the activity of the synthesing enzyme, phenylethanolamine-N-methyltransferase, depends on the high concentration of cortisol that drains from the cortex to the medulla.^[76]^[77]^[78]

Terminology

Epinephrine is the hormone's United States Adopted Name and International Nonproprietary Name, though the more generic name adrenaline is frequently used. The term Epinephrine was coined by the pharmacologist John Abel (from the Greek for "on top of the kidneys"), who used the name to describe the extracts he prepared from the adrenal glands as early as 1897.^[79] In 1901, Jokichi Takamine patented a purified adrenal extract, and called it "adrenalin" (from the Latin for "on top of the kidneys"), which was trademarked by Parke, Davis & Co in the U.S.^[79] In the belief that Abel's extract was the same as Takamine's, a belief since disputed, epinephrine became the generic name in the U.S.^[79] The British Approved Name and European Pharmacopoeia term for this chemical is adrenaline and is indeed now one of the few differences between the INN and BAN systems of names.^[80]

Among American health professionals and scientists, the term epinephrine is used over adrenaline. However, pharmaceuticals that mimic the effects of epinephrine are often called adrenergics, and receptors for epinephrine are called adrenergic receptors or adrenoceptors.

Mechanism of action

Physiologic responses to epinephrine by organ
Organ	Effects
Heart	Increases heart rate
Lungs	Increases respiratory rate
Systemic	Vasoconstriction and vasodilation
Liver	Stimulates glycogenolysis
Systemic	Triggers lipolysis
Systemic	Muscle contraction

Play media

7x speed timelapse video of fish melanophores responding to 200uM adrenaline.

As a hormone, epinephrine acts on nearly all body tissues. Its actions vary by tissue type and tissue expression of adrenergic receptors. For example, high levels of epinephrine causes smooth muscle relaxation in the airways but causes contraction of the smooth muscle that lines most arterioles.

Epinephrine acts by binding to a variety of adrenergic receptors. Epinephrine is a nonselective agonist of all adrenergic receptors, including the major subtypes α₁, α₂, β₁, β₂, and β₃.^[30] Epinephrine's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle,^[81] and stimulates glycolysis and inhibits insulin-mediated glycogenesis in muscle.^[82]^[83] β-Adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together, these effects lead to increased blood glucose and fatty acids, providing substrates for energy production within cells throughout the body.^[83]

Its actions are to increase peripheral resistance via α₁receptor-dependent vasoconstriction and to increase cardiac output via its binding to β₁ receptors. The goal of reducing peripheral circulation is to increase coronary and cerebral perfusion pressures and therefore increase oxygen exchange at the cellular level.^[84] While epinephrine does increase aortic, cerebral, and carotid circulation pressure, it lowers carotid blood flow and end-tidal CO₂ or E_TCO₂ levels. It appears that epinephrine may be improving macrocirculation at the expense of the capillary beds where actual perfusion is taking place.^[85]

Measurement in biological fluids

Epinephrine may be quantified in blood, plasma, or serum as a diagnostic aid, to monitor therapeutic administration, or to identify the causative agent in a potential poisoning victim. Endogenous plasma epinephrine concentrations in resting adults are normally less than 10 ng/L, but may increase by 10-fold during exercise and by 50-fold or more during times of stress. Pheochromocytoma patients often have plasma adrenaline levels of 1000–10,000 ng/L. Parenteral administration of epinephrine to acute-care cardiac patients can produce plasma concentrations of 10,000 to 100,000 ng/L.^[86]^[87]

Biosynthesis and regulation

In chemical terms, epinephrine is one of a group of monoamines called the catecholamines. It is produced in some neurons of the central nervous system, and in the chromaffin cells of the adrenal medulla from the amino acids phenylalanine and tyrosine.^[88]

Epinephrine is synthesized in the medulla of the adrenal gland in an enzymatic pathway that converts the amino acid tyrosine into a series of intermediates and, ultimately, epinephrine. Tyrosine is first oxidized to L-DOPA, which is subsequently decarboxylated to give dopamine. Oxidation gives norepinephrine. The final step in epinephrine biosynthesis is the methylation of the primary amine of noradrenaline. This reaction is catalyzed by the enzyme phenylethanolamine N-methyltransferase (PNMT) which utilizes S-adenosylmethionine (SAMe) as the methyl donor.^[89] While PNMT is found primarily in the cytosol of the endocrine cells of the adrenal medulla (also known as chromaffin cells), it has been detected at low levels in both the heart and brain.^[90]

Regulation

The major physiologic triggers of adrenaline release center upon stresses, such as physical threat, excitement, noise, bright lights, and high ambient temperature. All of these stimuli are processed in the central nervous system.^[91]

Adrenocorticotropic hormone (ACTH) and the sympathetic nervous system stimulate the synthesis of adrenaline precursors by enhancing the activity of tyrosine hydroxylase and dopamine-β-hydroxylase, two key enzymes involved in catecholamine synthesis.^{[citation needed]} ACTH also stimulates the adrenal cortex to release cortisol, which increases the expression of PNMT in chromaffin cells, enhancing adrenaline synthesis. This is most often done in response to stress.^{[citation needed]} The sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of adrenaline. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and, thus, the release of adrenaline (and noradrenaline) into the bloodstream.^{[citation needed]}

Unlike many other hormones adrenaline (as with other catecholamines) does not exert negative feedback to down-regulate its own synthesis.^[92] Abnormally elevated levels of adrenaline can occur in a variety of conditions, such as surreptitious epinephrine administration, pheochromocytoma, and other tumors of the sympathetic ganglia.

Its action is terminated with reuptake into nerve terminal endings, some minute dilution, and metabolism by monoamine oxidase and catechol-O-methyl transferase.

History

Extracts of the adrenal gland were first obtained by Polish physiologist Napoleon Cybulski in 1895. These extracts, which he called nadnerczyna, contained adrenaline and other catecholamines.^[93] American ophthalmologist William H. Bates discovered adrenaline's usage for eye surgeries prior to 20 April 1896.^[94] Japanese chemist Jokichi Takamine and his assistant Keizo Uenaka independently discovered adrenaline in 1900.^[95]^[96] In 1901, Takamine successfully isolated and purified the hormone from the adrenal glands of sheep and oxen.^[97] Adrenaline was first synthesized in the laboratory by Friedrich Stolz and Henry Drysdale Dakin, independently, in 1904.^[96]

Society and culture

Names

Names for epinephrine include adrenaline, adrenalin, and β,3,4-trihydroxy-N-methylphenethylamine.

Epinephrine is available in an autoinjector delivery system. Twinject, which is now discontinued, contained a second dose of adrenaline in a separate syringe and needle delivery system contained within the body of the autoinjector. Though both EpiPen and Twinject are trademark names, common usage of the terms is drifting toward the generic context of any adrenaline autoinjector.^{[citation needed]}

Strength

Adrenaline has been implicated in feats of great strength, often occurring in times of crisis.^[98]^[99]

References

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General references

Boron WF, Boulpaep EL (2005). Medical Physiology: A Cellular And Molecular Approach. Philadelphia, PA: Elsevier/Saunders. ISBN 1-4160-2328-3. OCLC 56191776.
Voet D, Voet J (2004). Biochemistry (3rd ed.). USA: Wiley. ISBN 0-471-19350-X. OCLC 154657578.

Jessop, D and Grossman, A The Discovery of Adrenaline

External links

U.S. National Library of Medicine: Drug Information Portal – Epinephrine
BrainImmune.com, BrainImmune – a web-based resource in neuroendocrine-immunology and stress-immune interactions

English Journal

[Effects of chronic intermittent hypobaric hypoxia on immune function in rat].

Shi M1, Cui F, Yang CY, Zhang H, Wang YP, Wei L, Zhou ZN, Zhang Y.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology.Zhongguo Ying Yong Sheng Li Xue Za Zhi.2009 Nov;25(4):433-8.
AIM: To elucidate the effect of CIHH on cellular immunity and humoral immunity in rat by using flow cytometry method, immunohistochemistry method and electron microscopy techniques.METHODS: Forty-eight male adult Sprague-Dawley rats were randomly divided into 4 groups: control(CON) group, 14 days CI
PMID 21158023

[The effect of the local anesthesia to the posterior ramus of the mandible in patients with temporomandibular joint problems].

Kimura S1, Hatano Y, Yokozuka S.
Shigaku = Odontology; journal of Nihon Dental College.Shigaku.1990 Jun;78(1):63-82.
Some clinicians in North America use anesthetic injections to differentiate the symptoms such as pain and stiffness in the facial area and neck in patients with TMJ problems. However, the effects and area which is influenced have not been studied. The purpose of this study was to study procedures an
PMID 2134959

THE EFFECT OF SEROTONIN INJECTED INTRAARTERIALLY ON THE CUTANEOUS NERVE ADDITIONALLY CONTRASTED WITH NOR-EPIRENAMINE.

ONOGI H.
Nagoya journal of medical science.Nagoya J Med Sci.1965 Jul;27:185-200.
PMID 14338192

Japanese Journal

気管支喘息患者におけるアドレナリン投与時の血糖, 乳酸, 焦性ブドウ酸および血漿Cyclic AMP値の変動について

富澤古志郎
アレルギー 27(8), 687-696, 713-714, 1978-08-30
気管支喘息患者におけるβアドレナリン刺激に対する反応を明らかにするために本研究をおこなつた.著者はアドレナリン投与時の血糖, 乳酸, 焦性ブドウ酸値を喘息患者37例と健常者20例について比較検討し, さらに喘息患者の重症度, 病型の面より検討した.アドレナリン投与時の血漿 cyclic AMP (cAMP) 値は喘息患者5例と健常者5例について比較検討した.アドレナリン投与量は7μg/kgである. …
NAID 110002411142

腺腫を有する前立腺の血液循環に対するX線学的研究

岡直友,杉浦弌,和志田裕人
日本泌尿器科學會雜誌 63(3), 229-234, 1972-03
… For this purpose, we have examined the effect of epirenamine, a temporary but powerful vasoconstrictor, in the transrectal prostatograms which assures greater certainty of diagnosis. … We also hoped to evaluate the effect of epirenamine. … The effect of intra-prostatic epirenamine injection in transrectal prostatography was studied in benign prostatic hyperplasia. …
NAID 110003078301

「アドレナリン」

Epinephrine
Systematic (IUPAC) name
	(R)-4-(1-Hydroxy-2-(methylamino)ethyl)benzene-1,2-diol
Clinical data
Trade names	EpiPen, others
AHFS/Drugs.com	monograph
MedlinePlus	a603002
Licence data	US FDA:link
Pregnancy; category	US: C (Risk not ruled out); ;
Legal status	AU: S4 (Prescription only); UK: POM (Prescription only); US: Prescription only/OTC;
Addiction; liability	None
Routes of; administration	IV, IM, endotracheal, IC, nasal, eye drop
Pharmacokinetic data
Metabolism	adrenergic synapse (MAO and COMT)
Onset of action	Rapid
Biological half-life	2 minutes
Duration of action	Few minutes
Excretion	Urine
Identifiers
CAS Number	51-43-4
ATC code	A01AD01 B02BC09 C01CA24 R01AA14 R03AA01 S01EA01
PubChem	CID: 5816
IUPHAR/BPS	479
DrugBank	DB00668
ChemSpider	5611
UNII	YKH834O4BH
KEGG	D00095
ChEBI	CHEBI:28918
ChEMBL	CHEMBL679
PDB ligand ID	ALE (PDBe, RCSB PDB)
Chemical data
Formula	C9H13NO3
Molecular mass	183.204 g/mol
	SMILES Oc1ccc(cc1O)[C@@H](O)CNC ;
	InChI InChI=1S/C9H13NO3/c1-10-5-9(13)6-2-3-7(11)8(12)4-6/h2-4,9-13H,5H2,1H3/t9-/m0/s1 ; Key:UCTWMZQNUQWSLP-VIFPVBQESA-N ;
(verify)

　　[★]

英: adrenarine
同: (国試)エピネフリン epinephrine、エピレナミン epirenamine、スプラレニン suprarenin
化: 酒石酸水素エピネフリン
商: Adrenalin, EpiPen、ボスミン、エピペン
関: カテコールアミン、ノルアドレナリン、アドレナリン受容体

SPC. 61,68,86,142
GOO. 244

副腎髄質のクロム親和性細胞で合成・分泌される
MAOやCOMTによって代謝される

作用機序

薬理作用

血管作用

小動脈、前毛細血管括約筋？収縮
アドレナリン反転 epinephreine reversal

アドレナリン投与下にα受容体阻害薬を投与すると末梢血管抵抗が低下し血圧が低下する現象。α受容体を介した末梢血管収縮が抑制され、β2受容体を介した末梢血管平滑筋が弛緩することによる。

動態

適応

効能又は効果

(エピネフリン注０．１％シリンジ「テルモ」添付文書)

下記疾患に基づく気管支痙攣の緩解

気管支喘息，百日咳
各種疾患もしくは状態に伴う急性低血圧またはショック時の補助治療
心停止の補助治療

用量

心肺蘇生

ACLS：静注1mg　　←　　プレフィルのシリンジは大抵1mg/1mlで調製されている。
PALS：静注・骨髄 0.01mg/kg　気管内投与 0.1mg/kg

アナフィラキシーショック：皮下注～筋注で0.3mg

注意

本剤は心筋酸素需要を増加させるため、心原性ショックや出血性・外傷性ショック時の使用は避けること(エピネフリン注０．１％シリンジ「テルモ」添付文書)

禁忌

副作用

「norepirenamine」

　　[★] ノルアドレナリン、ノルエピレナミン

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リンク元	「アドレナリン」
拡張検索	「norepirenamine」

匿名

検索

案内

epirenamine