Prajmaline (Neo-gilurythmal)[1] is a class Iaantiarrhythmic 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 ofajmaline, with a higher bioavailability than its predecessor.[5] It acts to stoparrhythmias of the heart through a frequency-dependent block of cardiac sodium channels.[2]
Prajmaline 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.
The 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]
Prajmaline 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]
The 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]
There 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]
An 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]
Due 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]
^abcKöppel C, Oberdisse U, Heinemeyer G (1990). "Clinical course and outcome in class IC antiarrhythmic overdose".Clinical Toxicology.28 (4):433–44.doi:10.3109/15563659009038586.PMID2176700.
^Milne JR, Hellestrand KJ, Bexton RS, Burnett PJ, Debbas NM, Camm AJ (February 1984). "Class 1 antiarrhythmic drugs--characteristic electrocardiographic differences when assessed by atrial and ventricular pacing".European Heart Journal.5 (2):99–107.doi:10.1093/oxfordjournals.eurheartj.a061633.PMID6723689.
^Hinse C, Stöckigt J (July 2000). "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)".Die Pharmazie.55 (7):531–2.PMID10944783.
^abLangenfeld H, Köhler C, Weirich J, Kirstein M, Kochsiek K (November 1992). "Reverse use dependence of antiarrhythmic class Ia, Ib, and Ic: effects of drugs on the action potential duration?".Pacing and Clinical Electrophysiology.15 (11 Pt 2):2097–102.doi:10.1111/j.1540-8159.1992.tb03028.x.PMID1279606.S2CID25864256.
^abcdefSowton E, Sullivan ID, Crick JC (1984). "Acute haemodynamic effects of ajmaline and prajmaline in patients with coronary heart disease".European Journal of Clinical Pharmacology.26 (2):147–50.doi:10.1007/bf00630278.PMID6723753.S2CID20512025.
^abcdHandler CE, Kritikos A, Sullivan ID, Charalambakis A, Sowton E (1985). "Effects of oral prajmaline bitartrate on exercise test responses in patients with coronary artery disease".European Journal of Clinical Pharmacology.28 (4):371–4.doi:10.1007/bf00544352.PMID4029242.S2CID521671.
^abMalek SA, Adorante JS, Stys PK (March 2005). "Differential effects of Na-K-ATPase pump inhibition, chemical anoxia, and glycolytic blockade on membrane potential of rat optic nerve".Brain Research.1037 (1–2):171–9.doi:10.1016/j.brainres.2005.01.003.PMID15777766.S2CID29226181.
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