Although it has been well known that ventricular fibrillation is the most important complication during hypothermia, much investigation has failed to show the exact nature of the etiology of ventricular fibrillation. Recently, there has been considerable research on the relationship between sympathetic activity and ventricular fibrillation under hypothermia. Cardiac muscle normally contains a certain amount of norepinephrine and the dramatic effect of this catecholamines on the cardiac muscle is well documented. It is, therefore, conceivable that cardiac catecholamines might exert an influence on the susceptibility of heart muscle to tachycardia, ventricular fibrillation and arrhythmia, under hypothermia. Hypothermia itself is stress enough to increase tonus of sympatheticoadrenal system. The normal heart is supplied by an autonomic innervation and is subjected to action of circulating catecholamines which may be released from the heart. If the reaction of the heart associated with a variable amount of cardiac catecholamines is. permitted to occur in the induction of hypothermia, the action of this agent on the heart has not to be differentiated from the direct effects of cooling. The studies presented in this paper were designed to provide further information about the cardio-physiological effects of reduced body temperature, with special reference to the role of catecholamines in ventricular fibrillation. Healthy cats, weighing about 3 kg, were anesthetized with pentobarbital(30 mg/kg) intraperitoneally. The trachea was intubated and the endotracheal tube was connected to a C.F. Palmer type A.C. respirator. Hypothermia was induced by immersing the cat into a ice water tub and the rate of body temperature lowering was $1^{\circ}C$ per 5 to 8 min. Esophageal temperature and ECG (Lead II) were simultaneously monitored. In some cases the blood pH and serum sodium and potassium were estimated before the experiment. After the experiment the animals were killed and the hearts were excised. The catecholamines content of the cardiac muscle was measured by the method of Shore and Olin (1958). The results obtained are summarized as follows. 1) In control animal the heart rate was slowed as the temperature fell and the average pulse rates of eight animals were read 94/min at $31^{\circ}C$, 70/min at $27^{\circ}C$ and 43/min at $23^{\circ}C$ if esophageal temperature. Ventricular fibrillation was occurred with no exception at a mean temperature of $20.3^{\circ}C(21-l9^{\circ}C)$. The electrocardiogram revealed abnormal P waves in each progressive cooling of the heart. there was, ultimately, a marked delay in the P-R interval, QRS complex and Q-T interval. Inversion of the T waves was characteristic of all animals. The catecholamines content of the heart muscle excised immediately after the occurrence of ventricular fibrillation was about thirty percent lower than that of the pre-hypothermic heart, that is, $1.0\;{\mu}g/g$ wet weight compared to the prehypothermic value of $1.41\;{\mu}g/g$ wet weight. The changes of blood pH, serum sodium and potassium concentration were not remarkable. 2) By the adrenergic receptor blocking agent, DCI(2-3 mg/kg), given intramuscularly thirty minutes before hypothermia, ventricular fibrillation did not occur in one of five animals when their body temperature was reduced even to $16^{\circ}C$. These animals succumbed at that low temperature, and the changes of heart rate and loss of myocardial catecholamines after hypothermia were similar to those of normal animals. The actual effect of DCI preventing the ventricular fibrillation is not predictable. 3) Administration of reserpine(1 mg/kg, i.m.) 24 hours Prior to hypothermia disclosed reduced incidence of ventricular fibrillation, that is, six of the nine animals went into fibrillation at an average temperature of $19.6^{\circ}C$. By reserpine myocardial catecholamines content dropped to $0.045\;{\mu}g/g$ wet weight. 4) Bretylium pretreatment(20 mg/kg, i.m.), which blocks the release of catecholamines, Prevented the ventricular fibrillation under hypothermia in four of the eight cats. The pulse rate, however, was approximately the same as control and in some cases was rather slower. 5) Six cats treated with norepinephrine(2 mg/kg, i.m.) or DOPA(50 mg/kg) and tranylcypromine(10 mg/kg), which tab teen proved to cause significant increase in the catecholamines content of the heart muscle, showed ventricular fibrillation in all animals under hypothermia at average temperature of $21.6^{\circ}C$ and the pulse rate increased remarkably as compared with that of normal. Catecholamines content of cardiac muscle of these animals markedly decreased after hypothermia but higher than control animals. 6) The functional refractory periods of isolated rabbit atria, determined by the paired stimulus technique, was markedly shortened by administration of epinephrine, norepinephrine and isoproterenol. 7) Adrenergic beta-blocking agents, such as pronethalol, propranolol and sotalol(MJ-1999), inhibited completely the shortening of refractory period induced by norepinephrine. 8) Pretreatment with either phenoxftenbamine or phentolamine, an adrenergic alphatlocking agent, did not modify the decrease in refractory period induced by norepinephrine. From the above experiment it is possible to conclude that catecholamines play an important role in producing ventricular fibrillation under hypothermia. The shortening of the refractorf period of cardiac muscle induced by catecholamines mar be considered as a partial factor in producing ventriculr fibrillaton and to be mediated by beta-adrenergic receptor.