Molsidomine was administered sub-lingually to two groups of five patients. One group had normal left ventricular function and the other had abnormal left ventricular function. Molsidomine was found to induce a decrease in the left ventricular filling pressure and volume and an increase in ventricular distensibility. It helps reduce the pre-load on the ventricle and parietal rigidity. It also reduces systemic blood pressure and resistance as well as the parietal pressure and the total systolic load opposing ejection. It helps reduce the post-load and the metabolic requirements of the myocardium. It does not have any depressant action on the myocardium, even when the ventricular function was initially abnormal. The action of the molecule is apparent between the 20th and the 30th minute and is maximal at the 40th minute, which was the limit of the experiment. The tolerance of the product was excellent in these ten subjects.
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