Abstract
The effects of chloracyzine (2-chloro-10-(3-diethylaminopropionyl)-phenothiazine hydrochloride; antianginal drug) on myocardial oxygen consumption were studied in open-chest cats and cat isolated hearts using oximetry and polarography respectively. It was found that chloracyzine produced a decrease in myocardial oxygen consumption accompanied by a reduction in coronary blood flow preceded by transient coronary dilatation. Chloracyzine produced an insignificant increase in arterial pressure; heart rate increased slightly in the open-chest experiments but not in the isolated heart. It is suggested that reduced oxygen uptake after chloracyzine is realized through improved efficiency in the use of oxygen.
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