ANTAGONIZING SUBSTANCES OBTAINED FROM WHALE HEART EXTRACT TO VASOPRESSIN INDUCED MYOCARDIAL HYPOXIA

Abstract

There are several reports that a protein-free extract of heart muscles from mammalian animals dilates coronary vessels (1, 2), increases the amplitude of heart (3), and improves the efficiency of contractions in heart lung preparations (4). Clinically, the extract has been used as an antianginal drug (5, 6), and a drug for heart failure contradictorily (7, 8). One of the main approaches to antianginal drugs has been studies of coronary dilators. However, the majority of pharmacological studies have been carried out in animals with a normal coronary circulation and the results obtained may not predict the status of the abnormal coronary circulation. Certainly, studies in man indicate that the coronary bed of the anginal patient is incapable of dilatation so that nitroglycerin produces no increase in coronary flow (9, 10). Furthermore, some reports show that dipyridamol having specific potent coronary vasodilating activity is not effective for angina pectoris (11-13). Thus, many other approaches have been tried to investigate antianginal drugs. Clinically, ST segment depression in electrocadiogram of patients of angina pectoris is very common phenomenon, and we consider ST segment depression in rats produced with vasopressin or adrenaline might be one of the experimental models of angina pectoris. Lindner et al. have shown that the vasopressin induced ischemia of the dog heart was improved after three daily injections of the large doses of a heart extract (14). Black have shown that oral administration of a heart extract for two weeks produced improvement on the above mentioned ischemia in rabbits (15). This paper describes a modification of similar experimental methods in rats and the identification of components which improves the ST segment depression in the heart extract.