Enoximone belongs to the
imidazole class of compounds, that possess positive inotropic and vasodilatory activities. These pharmacologic effects are caused by selective inhibition of a cAMP-specific
phosphodiesterase in the heart and in the smooth muscle of blood vessels. Results obtained in intact animals showed a dose-dependent increase in cardiac contractile force and a reduction in peripheral arterial resistance with only a slight increase in heart rate. Following acute administration of
enoximone to patients suffering from
cardiac failure an almost linear increase of cardiac index with increasing doses was found.
Enoximone is eliminated from the body by biotransformation.
Sulfoxide formation is the main metabolic step in man. This metabolite is excreted in the urine.
Enoximone sulfoxide also possesses some
cardiotonic activity. Reconversion of
enoximone sulfoxide to
enoximone was shown to occur in the liver and, to some extent, also in the kidney. Bioavailability of
enoximone after a single oral dose of 3 mg/kg is about 55%, but may be higher following chronic
therapy. This is probably due to saturation of the first-pass metabolism. A mean clearance of about 10 ml/min/kg and a mean half-life of 6 h were determined in patients with
cardiac failure. These values are different from those measured in normal volunteers, indicating a reduced clearance of
enoximone in these patients. In patients with
renal failure enoximone sulfoxide accumulates in plasma. The elimination of
enoximone is also reduced which might be caused by reconversion of
enoximone sulfoxide to
enoximone in this pathophysiologic condition. Thus, the dose of
enoximone should be reduced in patients with severe impairment of renal function. Clinically significant drug interactions have not been reported so far.