Abstract
It is now well recognized that taurine is a constituent of cardiac muscle, comprising over 50% of the free amino acid pool of this tissue (Jacobsen and Smith, 1968). However, the function of taurine in heart is not known. The initial stimulus to investigate the role of taurine in cardiac tissue was the pioneering work of Read and Welty (1963; Welty and Read, 1963). These workers reported that intravenous administration of taurine to dogs resulted in the disappearance of arrhythmias induced by large doses of epinephrine and digoxin. Supporting data for the role of taurine as an antiarrhythmic agent have been reported by Novelli et al. (1969) and Guidotti and Giotti (1970). However, it was the observations of Chazov et al. (1974) that fortified the potential role of taurine as an antiarrhythmic agent. Taurine was shown to “normalize” the electrocardiographic abnormalities produced by toxic doses of strophanthin-K in isolated perfused guinea pig hearts and in dogs in vivo. While the above results have stimulated much thought, they are not without criticism. First, the interpretation of the effects of taurine on the abnormal electrocardiogram has been challenged by Hinton et al. (1975), who reported that taurine was ineffective in counteracting ventricular arrhythmias induced by deslanoside in the cat.
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