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The observations that digitalis exerts a positive inotropic effect on the cat papillary muscle (1) and on the tortoise ventricle (2) led to the view, now generally accepted, that the salutary clinical and hemodynamic effects of this drug in congestive heart failure result primarily from its direct stimulation of myocardial contraction (3). This concept has received support from hemodynamic studies in patients with heart failure, demonstrating that digitalization results in an augmentation of the cardiac output and a lowering of the end-diastolic pressure of the failing ventricle (4-9). Considerable confusion still exists, however, concerning the effects of digitalis on the nonfailing human heart, since in the absence of clinical heart failure acute digitalization either depresses the cardiac output slightly or produces no significant change in any hemodynamic parameter (6,8,(10)(11)(12)(13)(14). Such observations have led to the contention that digitalis does not stimulate the non-failing human heart (12,13,15,16).In the present investigation the direct effects of digitalis preparations on the contractile force of the non-failing human heart were measured with the Walton-Brodie strain gage arch (17). This instrument has been extensively utilized in the study of the effects of drugs on the heart both in the dog (18) and in man (19,20) (Table I). In 18 of these the drug was administered in the course of an open operation during total cardiopulmonary bypass. These 18 patients ranged from 4 to 40 years and averaged 22 years of age. Sixteen of the patients had atrial septal defects and 2 had valvular pulmonic stenosis. None of the patients had a history of congestive heart failure, and although several patients had experienced mild limitation of exercise, in none was this limitation even moderately severe. All were studied by cardiac catheterization before operation, and molderate pulmonary hypertension (systolic pressure greater than 40 mm Hg) was present in 3 of the 16 patients with atrial septal defect. In several of the subjects with this anomaly a small systolic pressure gradient between the right ventricle and the pulmonary artery existed, presumably due to the excessive blood flow across the pulmonic orifice. However, in no patient was the right ventricular end-diastolic pressure elevated above the upper limit of normal (5 mm Hg). Fourteen of the 18 patients who were studied while they were on cardiopulmonary bypass received acetylstrophanthidin, the total dose ranging from 0.5 to 1.5 mg (average 1.15 mg). This dose equaled 0.013 to 0.036 mg per kg and averaged 0.026 mg per kg or 0.155 cat units per kg body weight. In general, smaller doses of acetylstrophantlhidin were employed in the early portion of this study. When it became apparent that these doses resulted in no toxic effects they were gradually increased. Three of the other 4 patients digitalized while on cardiopulmonary bypass received 1.2 mg of lanatoside C, while the fourth patient received 0.80 mg of this glycoside. These doses equaled 0.021 to 0.0...

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