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ajmaline : ウィキペディア英語版
ajmaline

Ajmaline (also known by trade names Gilurytmal, Ritmos, and Aritmina) is an alkaloid that is class Ia antiarrhythmic agent. It is often used to bring out typical findings of ST elevations in patients suspected of having Brugada syndrome.
The compound was first isolated by Salimuzzaman Siddiqui in 1931 〔Siddiqui, S.; Siddiqui, R. H. (1931). ''J. Indian Chem. Soc.'' 8: 667–80.〕 from the roots of ''Rauwolfia serpentina''. He named it ''ajmaline'', after Hakim Ajmal Khan, one of the most illustrious practitioners of Unani medicine in South Asia.〔Ahmed Nasim Sandilvi (2003), (Salimuzzaman Siddiqui: pioneer of scientific research in Pakistan ). Daily Dawn. 12 April 2003. Retrieved on 19 July 2007.〕 Ajmaline can be found in most species of the ''Rauwolfia'' genus as well as ''Catharanthus roseus''.〔Roberts, M.F.; Wink, M. (1998), ''Alkaloids: Biochemistry, Ecology, and Medical applications''. Plenum Press.〕 In addition to Southeast Asia, Rauwolfia species have also been found in tropical regions of India, Africa, South America, and some oceanic islands. Other indole alkaloids found in Rauwolfia include reserpine, ajmalicine, serpentine, corynanthine, and yohimbine. While 86 alkaloids have been discovered throughout Rauvolfia vomitoria, ajmaline is mainly isolated from the stem bark and roots of the plant.〔
Due to the low bioavailability of ajmaline, a semisynthetic propyl derivative called prajmaline (trade name Neo-gilurythmal) was developed that induces similar effects to its predecessor but has better bioavailability and absorption.
==Mechanism of action==

Ajmaline was first discovered to lengthen the refractory period of the heart by blocking sodium ion channels,〔 but it has also been noted that it is also able to interfere with the hERG (human Ether-a-go-go-Related Gene) potassium ion channel. In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. When ajmaline reversibly blocks hERG, repolarization occurs more slowly because it is harder for potassium to get out due to less unblocked channels, therefore making the RS interval longer. Ajmaline also prolongs the QR interval since it can also act as sodium channel blocker, therefore making it take longer for the membrane to depolarize in the first case. In both cases, ajmaline causes the action potential to become longer. Slower depolarization or repolarization results in a lengthened QT interval (the refractory period), and therefore makes it take more time for the membrane potential to get below the threshold level so the action potential can be re-fired. Even if another stimulus is present, action potential cannot occur again until after complete repolarization. Ajmaline causes action potentials to be prolonged, therefore slowing down firing of the conducting myocytes which ultimately slows the beating of the heart.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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