| 词条 | Prajmaline |
| 释义 |
| Verifiedfields = changed | verifiedrevid = 464212942 | IUPAC_name = (4α,16R,17R,21α)-4-propylajmalan-4-ium-17,21-diol | image = Prajmaline.svg | tradename = | pregnancy_AU = | pregnancy_US = | pregnancy_category = | legal_AU = | legal_UK = | legal_US = | legal_status = | routes_of_administration = | bioavailability = | protein_bound = | metabolism = | elimination_half-life = | excretion = | CAS_number_Ref = {{cascite|changed|??}} | CAS_number = 35080-11-6 | ATC_prefix = C01 | ATC_suffix = BA08 | PubChem = 37042 | DrugBank_Ref = {{drugbankcite|correct|drugbank}} | DrugBank = | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} | ChemSpiderID = 16735977 | UNII_Ref = {{fdacite|correct|FDA}} | UNII = 75934UD4GJ | C=23 | H=33 | N=2 | O=2 | charge = + | molecular_weight = 369.520 g/mol | smiles = O[C@@H]6C4[C@@H]2C[C@]65c1ccccc1N(C)[C@H]5[C@@H]3C[C@H]4[C@H](CC)[C@@H](O)[N+]23CCC | StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI = 1S/C23H33N2O2/c1-4-10-25-17-11-14(13(5-2)22(25)27)19-18(25)12-23(21(19)26)15-8-6-7-9-16(15)24(3)20(17)23/h6-9,13-14,17-22,26-27H,4-5,10-12H2,1-3H3/q+1/t13-,14-,17-,18-,19?,20-,21+,22+,23+,25?/m0/s1 | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey = UAUHEPXILIZYCU-UUEXUKNBSA-N }}Prajmaline (Neo-gilurythmal)[1] is a class Ia antiarrhythmic agent[2] which has been available since the 1970s.[3] Class Ia drugs increase the time one action potential lasts in the heart.[4] Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor.[5] It acts to stop arrhythmias of the heart through a frequency-dependent block of cardiac sodium channels.[2] MechanismPrajmaline causes a resting block in the heart.[6] A resting block is the depression of a person's Vmax after a resting period. This effect is seen more in the atrium than the ventricle.[6] The effects of some Class I antiarrhythmics are only seen in a patient who has a normal heart rate (~1 Hz).[7] This is due to the effect of a phenomenon called reverse use dependence.[7] The higher the heart rate, the less effect Prajmaline will have. UsesThe drug Prajmaline has been used to treat a number of cardiac disorders. These include: coronary artery disease,[8][9] angina,[8][9] paroxysmal tachycardia and Wolff–Parkinson–White syndrome.[1] Prajmaline has been indicated in the treatment of certain disorders where other antiarrhythmic drugs were not effective.[1] AdministrationPrajmaline can be administered orally,[9] parenterally[8] or intravenously.[8] Three days after the last dose, a limited effect has been observed. Therefore, it has been suggested that treatment of arrhythmias with Prajmaline must be continuous to see acceptable results.[1] PharmacokineticsThe main metabolites of Prajmaline are: 21-carboxyprajmaline and hydroxyprajmaline. Twenty percent of the drug is excreted in the urine unchanged. Daily therapeutic dose is 40–80 mg. Distribution half-life is 10 minutes. Plasma protein binding is 60%. Oral bioavailability is 80%. Elimination half-life is 6 hours. Volume of distribution is 4-5 L/kg. [3]Side EffectsThere are no significant adverse side-effects of Prajmaline when taken alone and with a proper dosage.[1][8][9] Patients who are taking other treatments for their symptoms (e.g. beta blockers and nifedipine) have developed minor transient conduction defects when given Prajmaline.[8] OverdoseAn overdose of Prajmaline is possible. The range of symptoms seen during a Prajmaline overdose include: no symptoms, nausea/vomiting, bradycardia, tachycardia, hypotension, and death.[3] Other Potential UsesDue to Prajmaline's sodium channel-blocking properties, it has been shown to protect rat white matter from anoxia (82 +/- 15%).[10][11] The concentration used causes little suppression of the preanoxic response.[10][11] References1. ^1 2 3 4 {{cite journal |vauthors=Janicki K, Orski J, Kakol J |title=[Antiarrhythmic effects of prajmaline (Neo-Gilurythmal) in stable angina pectoris in light of Holter electrocardiographic monitoring] |language=Polish |journal=Przegląd Lekarski |volume=52 |issue=10 |pages=485–491 |year=1995 |pmid=8834838}} {{Antiarrhythmic agents}}2. ^1 {{cite journal |vauthors=Weirich J, Antoni H |title=Differential analysis of the frequency-dependent effects of class 1 antiarrhythmic drugs according to periodical ligand binding: implications for antiarrhythmic and proarrhythmic efficacy |journal=Journal of Cardiovascular Pharmacology |volume=15 |issue=6 |pages=998–1009 | date=June 1990 |pmid=1694924 |doi=10.1097/00005344-199006000-00019}} 3. ^1 2 {{cite journal |vauthors=Köppel C, Oberdisse U, Heinemeyer G |title=Clinical course and outcome in class IC antiarrhythmic overdose |journal=Clinical Toxicology |volume=28 |issue=4 |pages=433–44 |year=1990 |pmid=2176700 |doi=10.3109/15563659009038586}} 4. ^{{cite journal |vauthors=Milne JR, Hellestrand KJ, Bexton RS, Burnett PJ, Debbas NM, Camm AJ |title=Class 1 antiarrhythmic drugs--characteristic electrocardiographic differences when assessed by atrial and ventricular pacing |journal=European Heart Journal |volume=5 |issue=2 |pages=99–107 | date=February 1984 |pmid=6723689 |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=6723689 |doi=10.1093/oxfordjournals.eurheartj.a061633}} 5. ^{{cite journal |vauthors=Hinse C, Stöckigt J |title=The structure of the ring-opened N beta-propyl-ajmaline (Neo-Gilurytmal) at physiological pH is obviously responsible for its better absorption and bioavailability when compared with ajmaline (Gilurytmal) |journal=Die Pharmazie |volume=55 |issue=7 |pages=531–2 | date=July 2000 |pmid=10944783}} 6. ^1 {{cite journal |vauthors=Langenfeld H, Weirich J, Köhler C, Kochsiek K |title=Comparative analysis of the action of class I antiarrhythmic drugs (lidocaine, quinidine, and prajmaline) in rabbit atrial and ventricular myocardium |journal=Journal of Cardiovascular Pharmacology |volume=15 |issue=2 |pages=338–45 | date=February 1990 |pmid=1689432 |doi=10.1097/00005344-199002000-00023}} 7. ^1 {{cite journal |vauthors=Langenfeld H, Köhler C, Weirich J, Kirstein M, Kochsiek K |title=Reverse use dependence of antiarrhythmic class Ia, Ib, and Ic: effects of drugs on the action potential duration? |journal=Pacing and Clinical Electrophysiology |volume=15 |issue=11 Pt 2 |pages=2097–102 | date=November 1992 |pmid=1279606 |doi=10.1111/j.1540-8159.1992.tb03028.x}} 8. ^1 2 3 4 5 {{cite journal |vauthors=Sowton E, Sullivan ID, Crick JC |title=Acute haemodynamic effects of ajmaline and prajmaline in patients with coronary heart disease |journal=European Journal of Clinical Pharmacology |volume=26 |issue=2 |pages=147–50 |year=1984 |pmid=6723753 |doi=10.1007/bf00630278}} 9. ^1 2 3 {{cite journal |vauthors=Handler CE, Kritikos A, Sullivan ID, Charalambakis A, Sowton E |title=Effects of oral prajmaline bitartrate on exercise test responses in patients with coronary artery disease |journal=European Journal of Clinical Pharmacology |volume=28 |issue=4 |pages=371–4 |year=1985 |pmid=4029242 |doi=10.1007/bf00544352}} 10. ^1 {{cite journal |author=Stys PK |title=Protective effects of antiarrhythmic agents against anoxic injury in CNS white matter |journal=Journal of Cerebral Blood Flow and Metabolism |volume=15 |issue=3 |pages=425–32 | date=May 1995 |pmid=7714000 |doi=10.1038/jcbfm.1995.53}} 11. ^1 {{cite journal |vauthors=Malek SA, Adorante JS, Stys PK |title=Differential effects of Na-K-ATPase pump inhibition, chemical anoxia, and glycolytic blockade on membrane potential of rat optic nerve |journal=Brain Research |volume=1037 |issue=1–2 |pages=171–9 | date=March 2005 |pmid=15777766 |doi=10.1016/j.brainres.2005.01.003}} 3 : Alkaloids|Sodium channel blockers|Alcohols |
| 随便看 |
|
开放百科全书收录14589846条英语、德语、日语等多语种百科知识，基本涵盖了大多数领域的百科知识，是一部内容自由、开放的电子版国际百科全书。