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Heparinization, started one hour following coronary ligation, was maintained for twenty-four hours. One week after recovery the hearts were perfused in vivo with india ink. After clearing, the proportion of ventricular mass infarcted was determined. No appreciable difference from the control series was found.SOLANDT and Best' found that coronary artery thrombosis, and consequent myocardial infarction, did not occur in 11 of 12 dogs when a sclerosing solution was introduced into a segment of coronary artery after beginning a twenty-four-hour period of heparinization. The heparin was diluted to 0.02 per cent in physiologic saline solution. Clotting time was determined by allowing 1.0 cc. of blood to drop from the Vinylite cannula into a clean, salinerinsed glass tube of 25-by 10-mm. capacity. Definite loss of fluidity, rather than clot formation, was taken as the end point. The clotting time was maintained usually at thirty to sixty minutes, the control readings varying from five to ten minutes. The clotting times were often erratic, frequently rising unexpectedly to from one hundred twenty to one hundred eighty minutes about eight hours after the infusion was started. Fatal intrathoracic hemorrhage usually occurred when such prolongation of clotting time was present, and also occurred when the prescribed dosage was exceeded because the clotting time apparently was below thirty minutes. The dogs were kept lightly narcotized with intravenous Nembutal, and the infusion of heparin was maintained for twenty-four hours. After. one week without medication, the dogs were sacrificed under morphine-Nembutal anesthesia. The sternum was split, the superior and inferior venae cavae were clamped, and, as the heart began to collapse, the aorta was clamped. Following the

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