- 同
- Beta-adrenergic receptor antagonists
WordNet
- to remain unmolested, undisturbed, or uninterrupted -- used only in infinitive form; "let her be"
- work in a specific place, with a specific subject, or in a specific function; "He is a herpetologist"; "She is our resident philosopher" (同)follow
- have life, be alive; "Our great leader is no more"; "My grandfather lived until the end of war" (同)live
- be identical to; be someone or something; "The president of the company is John Smith"; "This is my house"
- happen, occur, take place; "I lost my wallet; this was during the visit to my parents house"; "There were two hundred people at his funeral"; "There was a lot of noise in the kitchen"
- have the quality of being; (copula, used with an adjective or a predicate noun); "John is rich"; "This is not a good answer"
- occupy a certain position or area; be somewhere; "Where is my umbrella?" "The toolshed is in the back"; "What is behind this behavior?"
- spend or use time; "I may be an hour"
- stake on the outcome of an issue; "I bet $100 on that new horse"; "She played all her money on the dark horse" (同)wager, play
- the act of gambling; "he did it on a bet" (同)wager
- maintain with or as if with a bet; "I bet she will be there!" (同)wager
- second in order of importance; "the candidate, considered a beta male, was perceived to be unable to lead his party to victory"
- the 2nd letter of the Greek alphabet
- preliminary or testing stage of a software or hardware product; "a beta version"; "beta software"
- a class of drugs that inhibit (block) some biological process (同)blocking_agent
- a football player whose responsibility is to block players attempting to stop an offensive play
- beets (同)genus Beta
PrepTutorEJDIC
- 《連結語として補語を伴なって…『である』,…だ,…です / 《位置・場所を表す語句を伴って》(…に)『ある』,いる(occupy a place or situation) / 〈物事が〉『存在する』,ある(exist);〈生物が〉生存する,生きている(live) / 行われる,起こる,発生する(take place, occur) / 存続する,そのままでいる(remain as before) / 《『be to』 do》 / …する予定である,…することになっている / …すべきだ / 《受動態の不定詞を伴って》…できる / 《命令》…するのだ / 《条件節に》…する意図がある / 《『if…were to』 do》…するとしたなら / 《『be』 do『ing』》《進行形》 / 《進行中の動作》…している,しつつある / 《近い未来》…しようとしている,するつもり / 《動作の反復》(いつも)…している / 《『be』+『他動詞の過去分詞』》《受動態》…される,されている / 《『be』+『自動詞の過去分詞』》《完了形》…した[状態にある]
- 『かけ』・(…との)かけ《+『with』+『名』》 / かけた物(金) / かけの対象 / 〈金・物〉'を'『かける』 / (かけ事・ゲームなどで)〈人〉‘と'『かけをする』《+『名』〈人〉+『on』+『名』》 / (…に)『かける』《+『on』(『against』)+『名』(one's do『ing』)》
- ベータ(ギリシア語アルファベットの第2文字;B,β;英語のB,b に遭当)
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2018/03/31 08:27:50」(JST)
wiki en
| Beta blockers | |
|---|---|
| Drug class | |
|
Skeletal formula of propranolol, the first clinically successful beta blocker
|
|
| Class identifiers | |
| Synonyms | β-blockers, beta-adrenergic blocking agents, beta antagonists, beta-adrenergic antagonists, beta-adrenoreceptor antagonists, beta adrenergic receptor antagonists |
| Use | Hypertension, arrhythmia, etc. |
| ATC code | C07 |
| Biological target | beta receptors |
| Clinical data | |
| Drugs.com | Drug Classes |
| Consumer Reports | Best Buy Drugs |
| WebMD | MedicineNet RxList |
| External links | |
| MeSH | D000319 |
| In Wikidata | |
Beta blockers, also written β-blockers, are a class of medications that are particularly used to manage abnormal heart rhythms, and to protect the heart from a second heart attack (myocardial infarction) after a first heart attack (secondary prevention).[1] They are also widely used to treat high blood pressure (hypertension), although they are no longer the first choice for initial treatment of most patients.[2]
Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response.[3][4] Some block activation of all types of β-adrenergic receptors and others are selective for one of the three known types of beta receptors, designated β1, β2 and β3 receptors.[5] β1-adrenergic receptors are located mainly in the heart and in the kidneys.[4] β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.[4] β3-adrenergic receptors are located in fat cells.[6]
Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine (adrenaline). Beta blockers interfere with the binding to the receptor of epinephrine and other stress hormones, and weaken the effects of stress hormones.
In 1964, James Black[7] synthesized the first clinically significant beta blockers—propranolol and pronethalol; it revolutionized the medical management of angina pectoris[8] and is considered by many to be one of the most important contributions to clinical medicine and pharmacology of the 20th century.[9]
For the treatment of primary hypertension, meta-analyses of studies which mostly used atenolol have shown that although beta blockers are more effective than placebo in preventing stroke and total cardiovascular events, they are not as effective as diuretics, medications inhibiting the renin–angiotensin system (e.g., ACE inhibitors), or calcium channel blockers.[10][11][12][13]
Contents
- 1 Medical uses
- 1.1 Congestive heart failure
- 1.2 Anxiety
- 1.3 Cardiac surgery
- 2 Performance-enhancing use
- 3 Adverse effects
- 3.1 Contraindications
- 3.1.1 Asthma
- 3.1.2 Cocaine
- 3.2 Toxicity
- 3.1 Contraindications
- 4 β-Receptor antagonism
- 5 Intrinsic sympathomimetic activity
- 6 α1-receptor antagonism
- 7 Examples
- 7.1 Nonselective agents
- 7.2 β1-selective agents
- 7.3 β2-selective agents
- 7.4 β3-selective agents
- 8 Comparative information
- 8.1 Pharmacological differences
- 8.2 Indication differences
- 9 Other effects
- 10 See also
- 11 References
- 12 External links
Medical uses
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Large differences exist in the pharmacology of agents within the class, thus not all beta blockers are used for all indications listed below.
Indications for beta blockers include:
- Angina pectoris[14][15] (contraindicated for Prinzmetal's angina)
- Atrial fibrillation[16]
- Cardiac arrhythmia[vague]
- Congestive heart failure
- Essential tremor
- Glaucoma (As eye drops, they decrease intraocular pressure by lowering aqueous humor secretion.[17])
- Hypertension, although they are generally not preferred as an initial treatment.[18]
- Migraine prophylaxis
- Mitral valve prolapse
- Myocardial infarction
- Phaeochromocytoma, in conjunction with α-blocker
- Postural orthostatic tachycardia syndrome
- Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
- Theophylline overdose
Beta blockers have also been used for:
- Acute aortic dissection
- Hypertrophic obstructive cardiomyopathy
- Long QT syndrome
- Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications)
- Prevention of variceal bleeding in portal hypertension
- Possible mitigation of hyperhidrosis
- Social and other anxiety disorders
- Controversially, for reduction of perioperative mortality
Congestive heart failure
Although beta blockers were once contraindicated in congestive heart failure, as they have the potential to worsen the condition due to their effect of decreasing cardiac contractility, studies in the late 1990s showed their efficacy at reducing morbidity and mortality.[19][20][21] Bisoprolol, carvedilol, and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive heart failure, although at doses typically much lower than what are indicated for other conditions. Beta blockers are only indicated in cases of compensated, stable congestive heart failure; in cases of acute decompensated heart failure, beta blockers will cause a further decrease in ejection fraction, worsening the patient's current symptoms.
Beta blockers are known primarily for their reductive effect on heart rate, although this is not the only mechanism of action of importance in congestive heart failure.[citation needed] Beta blockers, in addition to their sympatholytic β1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering extracellular volume and increasing the oxygen-carrying capacity of blood. Heart failure characteristically involves increased catecholamine activity on the heart, which is responsible for a number of deleterious effects, including increased oxygen demand, propagation of inflammatory mediators, and abnormal cardiac tissue remodeling, all of which decrease the efficiency of cardiac contraction and contribute to the low ejection fraction.[22] Beta blockers counter this inappropriately high sympathetic activity, eventually leading to an improved ejection fraction, despite an initial reduction in ejection fraction.
Trials have shown beta blockers reduce the absolute risk of death by 4.5% over a 13-month period. In addition to reducing the risk of mortality, the numbers of hospital visits and hospitalizations were also reduced in the trials.[23]
Anxiety
Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration.[24] However, many controlled trials in the past 25 years indicate beta blockers are effective in anxiety disorders, though the mechanism of action is not known.[25] The physiological symptoms of the fight-or-flight response (pounding heart, cold/clammy hands, increased respiration, sweating, etc.) are significantly reduced, thus enabling anxious individuals to concentrate on the task at hand.
Musicians, public speakers, actors, and professional dancers have been known to use beta blockers to avoid performance anxiety, stage fright, and tremor during both auditions and public performances. The application to stage fright was first recognized in The Lancet in 1976, and by 1987, a survey conducted by the International Conference of Symphony Orchestra Musicians, representing the 51 largest orchestras in the United States, revealed 27% of its musicians had used beta blockers and 70% obtained them from friends, not physicians.[26] Beta blockers are inexpensive, said to be relatively safe, and on one hand, seem to improve musicians' performances on a technical level, while some, such as Barry Green, the author of "The Inner Game of Music" and Don Greene, a former Olympic diving coach who teaches Juilliard students to overcome their stage fright naturally, say the performances may be perceived as "soulless and inauthentic".[26]
Cardiac surgery
The use of beta blockers around the time of cardiac surgery decreases the risk of heart dysrhythmias.[27] Starting them around the time of other types of surgery, however, worsens outcomes.[27]
Performance-enhancing use
Because they promote lower heart rates and reduce tremors, beta blockers have been used in professional sports where high accuracy is required, including archery, shooting, golf[28] and snooker.[28] Beta blockers are banned by the International Olympic Committee.[29] In the 2008 Summer Olympics, 50-metre pistol silver medalist and 10-metre air pistol bronze medalist Kim Jong-su tested positive for propranolol and was stripped of his medals.[30]
For similar reasons, beta blockers have also been used by surgeons.[31]
Adverse effects
Adverse drug reactions associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema.[32] Due to the high penetration across the blood–brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other less lipophilic beta blockers to cause sleep disturbances, such as insomnia, vivid dreams and nightmares.[33]
Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with β1-selective (often termed "cardioselective") agents, but receptor selectivity diminishes at higher doses. Beta blockade, especially of the beta-1 receptor at the macula densa, inhibits renin release, thus decreasing the release of aldosterone. This causes hyponatremia and hyperkalemia.
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormone glucagon, which work together to increase plasma glucose. Therefore, blocking β2-adrenoceptors lowers plasma glucose. β1-blockers have fewer metabolic side effects in diabetic patients; however, the fast heart rate that serves as a warning sign for insulin-induced low blood sugar may be masked, resulting in hypoglycemia unawareness. This is termed beta blocker induced hypoglycemia unawareness. Therefore, beta blockers are to be used cautiously in diabetics.[34]
A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk of developing diabetes mellitus, while ACE inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers) actually decrease the risk of diabetes.[35] Clinical guidelines in Great Britain, but not in the United States, call for avoiding diuretics and beta blockers as first-line treatment of hypertension due to the risk of diabetes.[36]
Beta blockers must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta receptors increases blood pressure, reduces coronary blood flow, left ventricular function, and cardiac output and tissue perfusion by means of leaving the alpha-adrenergic system stimulation unopposed.[medical citation needed] Beta blockers with lipophilic properties and CNS penetration such as metoprolol and labetalol may be useful for treating CNS and cardiovascular toxicity from a methamphetamine overdose.[37] The mixed alpha- and beta blocker labetalol is especially useful for treatment of concomitant tachycardia and hypertension induced by methamphetamine.[38] The phenomenon of "unopposed alpha stimulation" has not been reported with the use of beta blockers for treatment of methamphetamine toxicity.[38] Other appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant overdose are vasodilators such as nitroglycerin, diuretics such as furosemide, and alpha blockers such as phentolamine.[39]
Contraindications
Asthma
Beta blockers are contraindicated in patients with asthma as stated in the British National Formulary 2011.[citation needed] The 2007 National Heart, Lung, and Blood Institute (NHLBI) asthma guidelines recommend against the use of non-selective beta blockers in asthmatics, while allowing for the use of cardioselective beta blockers.[40]
Cocaine
They should also be avoided in patients with a history of cocaine use or in cocaine-induced tachycardia.[citation needed]
Beta blockers should not be used as a first-line treatment in the acute setting for cocaine-induced acute coronary syndrome (CIACS). No recent studies have been identified that show the benefit of beta blockers in reducing coronary vasospasm, or coronary vascular resistance, in patients with CIACS. In the multiple case studies identified, the use of beta blockers in CIACS resulted in detrimental outcomes, and the discontinuation of beta blockers used in the acute setting led to improvement in clinical course.[citation needed] The guidelines by the American College of Cardiology/American Heart Association also support this idea, and recommend against the use of beta blockers in cocaine-induced ST-segment elevation myocardial infarction (MI) because of the risk of coronary vasospasm.[citation needed] Though, in general, beta blockers improve mortality in patients who have suffered MI, it is unclear whether patients with CIACS will benefit from this mortality reduction because no studies assess the use of beta blockers in the long term, and because cocaine users may be prone to continue to abuse the substance, thus complicating the effect of drug therapy.[41] Contrast media are not contraindicated in patients receiving beta blockers.[42]
Toxicity
Glucagon, used in the treatment of overdose,[43][44] increases the strength of heart contractions, increases intracellular cAMP, and decreases renal vascular resistance. It is, therefore, useful in patients with beta blocker cardiotoxicity.[45][46] Cardiac pacing is usually reserved for patients unresponsive to pharmacological therapy.
People experiencing bronchospasm due to the β2 receptor-blocking effects of nonselective beta blockers may be treated with anticholinergic drugs, such as ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Other antidotes for beta blocker poisoning are salbutamol and isoprenaline.
β-Receptor antagonism
Stimulation of β1 receptors by epinephrine and norepinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity.[47] Stimulation of β1 receptors on the kidney causes renin release.[48] Stimulation of β2 receptors induces smooth muscle relaxation,[49] induces tremor in skeletal muscle,[50] and increases glycogenolysis in the liver and skeletal muscle.[51] Stimulation of β3 receptors induces lipolysis.[52]
Beta blockers inhibit these normal epinephrine- and norepinephrine-mediated sympathetic actions,[3] but have minimal effect on resting subjects.[citation needed] That is, they reduce the effect of excitement or physical exertion on heart rate and force of contraction,[53] and also tremor,[54] breakdown of glycogen, and dilation of bronchi.[55]
Since β2 adrenergic receptors can cause vascular smooth muscle dilation, beta blockers may cause some vasoconstriction. However, this effect tends to be small because the activity of β2 receptors is overshadowed by the more dominant vasoconstricting α1 receptors. By far the greatest effect of beta blockers remains in the heart. Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors.[56]
Accordingly, nonselective beta blockers are expected to have antihypertensive effects.[57] The primary antihypertensive mechanism of beta blockers is unclear, but may involve reduction in cardiac output (due to negative chronotropic and inotropic effects).[58] It may also be due to reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity (for those beta blockers that do cross the blood–brain barrier, e.g. propranolol).
Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. Negative chronotropic properties of beta blockers allow the lifesaving property of heart rate control. Beta blockers are readily titrated to optimal rate control in many pathologic states.
The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade—resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties and prolongs action potential duration through potassium channel blockade.
Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin–angiotensin–aldosterone system, with a resultant decrease in blood pressure due to decreased sodium and water retention.
Intrinsic sympathomimetic activity
Also referred to as intrinsic sympathomimetic effect, this term is used particularly with beta blockers that can show both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker) and the concentration of the antagonized agent (usually an endogenous compound, such as norepinephrine). See partial agonist for a more general description.
Some beta blockers (e.g. oxprenolol, pindolol, penbutolol, labetalol and acebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low-level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.
Agents with ISA are not used after myocardial infarctions, as they have not been demonstrated to be beneficial. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia.[32]
α1-receptor antagonism
Some beta blockers (e.g., labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-adrenergic receptors, which provides additional arteriolar vasodilating action.[citation needed]
Examples
Dichloroisoprenaline, the first beta blocker
Nonselective agents
Nonselective beta blockers display both β1 and β2 antagonism.[59]
- Propranolol[59]
- Bucindolol (has additional α1-blocking activity)[60]
- Carteolol[61]
- Carvedilol (has additional α1-blocking activity)[59]
- Labetalol (has additional α1-blocking activity)[59]
- Nadolol[59]
- Oxprenolol (has intrinsic sympathomimetic activity)[62]
- Penbutolol (has intrinsic sympathomimetic activity)[59]
- Pindolol (has intrinsic sympathomimetic activity)[59]
- Sotalol (not considered a "typical beta blocker")[59]
- Timolol[59]
β1-selective agents
β1-selective beta blockers are also known as cardioselective beta blockers.[59]
- Acebutolol (has intrinsic sympathomimetic activity, ISA)[59]
- Atenolol[59]
- Betaxolol[59]
- Bisoprolol[59]
- Celiprolol (has intrinsic sympathomimetic activity)[63]
- Metoprolol[59]
- Nebivolol[59]
- Esmolol[64]
β2-selective agents
- Butaxamine[65]
- ICI-118,551[66]
β3-selective agents
- SR 59230A[67]
Comparative information
Pharmacological differences
- Agents with intrinsic sympathomimetic action (ISA)
- Acebutolol,[68] pindolol,[68] labetalol,[68] mepindolol,[69] oxprenolol,[62] celiprolol,[63] penbutolol[59]
- Agents organized by lipid solubility (lipophilicity)[70]
- High lipophilicity: propranolol, labetalol
- Intermediate lipophilicity: metoprolol, bisoprolol, carvedilol, acebutolol, timolol, pindolol
- Low lipophilicity (also known as hydrophilic beta blockers): atenolol, nadolol, and sotalol
- Agents with membrane stabilizing effect[71]
- Carvedilol, propranolol > oxprenolol > labetalol, metoprolol, timolol
Indication differences
- Agents specifically labeled for cardiac arrhythmia
- Esmolol,[72] sotalol,[73] landiolol (Japan)[74]
- Agents specifically labeled for congestive heart failure[59]
- Carvedilol, sustained-release metoprolol
- Agents specifically labeled for glaucoma
- Betaxolol,[71] carteolol,[71] levobunolol,[71] timolol,[71] metipranolol[75]
- Agents specifically labeled for myocardial infarction[59]
- Atenolol, metoprolol (immediate release), propranolol (immediate release), timolol, carvedilol (after left ventricular dysfunction)
- Agents specifically labeled for migraine prophylaxis[76]
- Timolol, propranolol
Propranolol is the only agent indicated for control of tremor, portal hypertension, and esophageal variceal bleeding, and used in conjunction with α-blocker therapy in phaeochromocytoma.[32]
Other effects
Beta blockers, due to their antagonism at beta-1 adrenergic receptors, inhibit both the synthesis of new melatonin and its secretion by the pineal gland. The neuropsychiatric side effects of some beta blockers (e.g. sleep disruption, insomnia) may be due to this effect.[77]
See also
- Alpha blockers
References
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External links
- Musicians and beta-blockers by Gerald Klickstein, March 11, 2010 (A blog post that considers "whether beta-blockers are safe, effective, and appropriate for performers to use.")
- Better Playing Through Chemistry by Blair Tindall, New York Times, October 17, 2004. (Discusses the use of beta blockers among professional musicians)
- Musicians using beta blockers by Blair Tindall. Condensed version of above article.
- In Defense of the Beta Blocker by Carl Elliott, The Atlantic, August 20, 2008. (Discusses the use of propranolol by a North Korean pistol shooter in the 2008 Olympics)
- beta-Adrenergic Blockers at the US National Library of Medicine Medical Subject Headings (MeSH)
Beta blockers (C07)
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|---|---|
| β, non-selective |
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| β1-selective |
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| β2-selective |
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| α1- + β-selective |
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Pharmacology: major drug groups
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|---|---|
| Gastrointestinal tract/ metabolism (A) |
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| Blood and blood forming organs (B) |
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| Cardiovascular system (C) |
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| Skin (D) |
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| Genitourinary system (G) |
|
| Endocrine system (H) |
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| Infections and infestations (J, P, QI) |
|
| Malignant disease (L01–L02) |
|
| Immune disease (L03–L04) |
|
| Muscles, bones, and joints (M) |
|
| Brain and nervous system (N) |
|
| Respiratory system (R) |
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| Sensory organs (S) |
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| Other ATC (V) |
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Sympatholytic (and closely related) antihypertensives (C02)
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| Sympatholytics (antagonize α-adrenergic |
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| Other antagonists |
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Drugs used for glaucoma preparations and miosis (S01E)
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| Sympathomimetics |
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| Parasympathomimetics |
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| Carbonic anhydrase inhibitors/ (sulfonamides) |
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| Beta blocking agents |
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| Prostaglandin analogues (F2α) |
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| Other agents |
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Adrenergic receptor modulators
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|---|---|
| α1 |
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| α2 |
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| β |
|
UpToDate Contents
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- 1. β遮断剤の主な副作用 major side effects of beta blockers
- 2. 駆出率低下を伴う心不全におけるβブロッカーおよびイバブラジンの使用 use of beta blockers and ivabradine in heart failure with reduced ejection fraction
- 3. 安定狭心症のマネージメントにおけるβ遮断剤 beta blockers in the management of stable angina pectoris
- 4. 急性冠症候群：β遮断剤の役割 acute myocardial infarction role of beta blocker therapy
- 5. 収縮能障害による心不全におけるβブロッカー使用の理論的根拠および臨床試験 rationale for and clinical trials of beta blockers in heart failure due to systolic dysfunction
English Journal
- Occurrence and ecotoxicological assessment of pharmaceuticals: Is there a risk for the Mediterranean aquatic environment?
- Desbiolles F1, Malleret L2, Tiliacos C3, Wong-Wah-Chung P4, Laffont-Schwob I5.
- The Science of the total environment.Sci Total Environ.2018 Oct 15;639:1334-1348. doi: 10.1016/j.scitotenv.2018.04.351. Epub 2018 May 26.
- PMID 29929299
- Natural history and predictors of mortality of patients with Takotsubo syndrome.
- Kim H1, Senecal C2, Lewis B3, Prasad A2, Rajiv G2, Lerman LO4, Lerman A5.
- International journal of cardiology.Int J Cardiol.2018 Sep 15;267:22-27. doi: 10.1016/j.ijcard.2018.04.139.
- PMID 29957259
- Advanced biological activated carbon filter for removing pharmaceutically active compounds from treated wastewater.
- Sbardella L1, Comas J2, Fenu A3, Rodriguez-Roda I4, Weemaes M3.
- The Science of the total environment.Sci Total Environ.2018 Sep 15;636:519-529. doi: 10.1016/j.scitotenv.2018.04.214. Epub 2018 Apr 30.
- PMID 29715656
Japanese Journal
- 臨床経験 レミフェンタニルを用いた麻酔管理において短時間作用型β遮断薬を必要とする因子の検討
- 岡田 真依,原 哲也,趙 成三 [他]
- 麻酔 62(9), 1112-1116, 2013-09
- NAID 40019794276
- 薬物治療 : β遮断薬 (特集 循環器疾患患者の外来管理)
- 猪又 孝元
- 循環器内科 73(3), 310-314, 2013-03
- NAID 40019623414
- 乳幼児ファロー四徴症におけるβ遮断薬服用と低血糖発作の頻度およびその危険因子の検討
- 伊藤 怜司,小川 潔,森 琢磨,菅本 健司,菱谷 隆,星野 健司,野村 耕司,関島 俊雄,目澤 秀俊,井田 博幸
- Pediatric Cardiology and Cardiac Surgery 29(3), 129-136, 2013
- 背景:β遮断薬は小児においても循環器疾患を中心に用いられるが,低血圧,徐脈,低血糖といった副作用が問題となることがある。特に低血糖は重大な後遺症を来す可能性があるが,小児における頻度や危険因子は明らかではない。目的:乳幼児ファロー四徴症におけるβ遮断薬服用の有無と低血糖発症の関連性を明らかにし,その危険因子を明らかにすること。方法:1983 年4 月～ 2011 年1 月に受診したファロー四徴症4 …
- NAID 130003380027
Related Links
- Beta-blockers are medicines used to treat high blood pressure, congestive heart failure, abnormal heart rhythms, and chest pain. ... Disclaimer The information in this Medicines for Cardiovascular Disease section has been taken from ...
- Beta Blockers Definition Beta blockers are medicines that affect the body's response to certain nerve impulses. This, in turn, decreases the force and rate of the heart's contractions, which lowers blood pressure and reduces the heart ...
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「blocker」
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- p adrenergic receptor antagonist(s)