Abstract-To determine whether or not the development of collateral channels can he accelerated by administration of vasodilators and whether the opening up of functional collateral channels is associated with an improved survival rate, a gradual occlusion of the major branches of the left coronary artery was produced in miniature swine with an Ameroid constrictor.Oral administration of drugs (twice a day) was started seven days before operation and was continued throughout the experimental period of 2 months. While the survival rate of the untreated animals was 6; 15 (40°;)), survival rates of animals treated with adenosine potentiators, dipyridamole and dilazep were 417 (57.1 °,;) and 5r7 (71.4°x;), respectively. However, a significant improvement of the survival rate was attained by KI 2119, survival rate was 617 (85.7 °0. Coronary angiography of the survived control animals revealed numerous, fine, collateral com munications between the left and right coronary arteries. Treatment with dipyridamole and dilazep resulted in formation of a dense network of thick collaterals.To quanti tate the degree of formation of the collateral channels, the anatomic anastomotic indices (AAI's) were calculated using histological specimens of the anterior free wall of the left ventricle. According to Menick et al. (16), AAI is a good measure of the functional capacity of the collateral vessels. AAI's of the animals treated with di pyridamole and dilazep were 2416.6_-=454.0 and 1864.7_x_ 248.3 as compared with 704.3--407.9 of the untreated animals. AAI's of the KI 2119-treated animals did not differ from those of the control animals. A linear correlation was observed between the survival rate and AAI's (r-0.74, p,--'0.05), indicating a close relationship between the survival rate and the development of functional collateral channels.It is generally accepted that well-developed and functional collateral arteries provide an effective defence against obstructive diseases of the coronary arteries.Although col laterals have been found in normal hearts of man (1-5), dog (6-8) and pigs (9-10), the functional capacity of these anastomoses is not sufliciently great to protect the heart from infarcts or ventricular fibrillation resulting from a sudden occlusion of the main trunks of the coronary arteries.For the collaterals to function as an efficient defence, a prior enlarge ment and growth of the pre-existing vessels is necessary, and such is effected by arterial hypoxia, anemia, and stenosis and occlusion of the coronary arteries. In addition, several