In acute experiments on the anesthetized dog, partial or complete occlusion of the left innominate vein resulting in a rise of pressure in the venous territory into which the thoracic duct drains, commensurate with the venous pressure rise seen in congestive heart failure, reduces the flow of lymph in the thoracic duct. This decrease in thoracic duct lymph flow is due, at least partially, to the accumulation of lymph in the lymphatic system and possibly the intercellular spaces. The present acute experiments suggest the possibility that this factor may play a role in the genesis of the systemic edema of chronic congestive heart failure, although only chronic experiments now under way will permit definitive conclusions.

In the anesthetized dog, experimentally induced ventricular tachycardia resulted initially in a very marked decrease in mean arterial blood pressure and cardiac output, then blood pressure and cardiac output rose and stabilized slightly below or markedly below their control levels. Such tachycardia resulted in a rise in the catecholamines blood level. Acute arteriovenous fistula resulting in a definite decrease in mean arterial blood pressure followed by complete or partial recovery of the blood pressure also resulted in an increase in the catecholamines blood level. The mechanisms, origin and role of this increase in catecholamines blood level are discussed.

It has been shown that electrically induced tachycardia of sufficiently high rate results in an immediate decrease of cardiac output and mean arterial blood pressure which recover partially or completely through both myocardial and vascular mechanisms ( 1,2 ) .Since during such bouts of tachycardia, there occurs a marked rise in the catecholamines blood level(2), it was thought of interest to investigate the importance of the adrenal medulla in the compensation of the cardiovascular system to induced tachycardia by studying the response of the cardiovascular system to tachycardia immediately before and after bilateral adrenalectomy, in order to gain more insight into the respective role of the adrenal medulla and the sympathetic nervous system.tMethods. Eleven dogs (22.3 kg-33.4 kg) were anesthetized by intravenous administration of 100 mg of chloralose per kg. The methods used to measure and record continuously the output of the left ventricle (CO) and mean arterial bIood pressure (MABP) as well as the formula used to calculate total * This work was supported by grants-in-aid from American Heart Assn., Life Insurance Medical Research Fund, St. Louis Heart Assn., and U. S. Public Health Service. t It seems legitimate to assume that the ablation of the adrenal ccrtex which was removed during tctal bilateral adrenalectomy played no role in the present acute experiments of very short duration, lasting approximately 22 to 59 minutes from the beginning of the first control period and 9 t o 47 minutes from the end of the adrenalectomy. Some of the postadrenalectomy bouts of tachycardia were initiated purposely this long after the end of the adrenalectomy to insure the disappearance from the blood of the catecholamines which might have been released in the blood stream during the adrenalectomy, although it is most unlikely that catecholamines were released into the blood stream during adrenalectomy with the technique used(3). peripheral resistance (TPR) have been described(4). Heart rate (HR) was determined from electrocardiographic tracings. To reduce to a minimum the extraneous effect of the surgical manoeuvres at the time of actual removal of the adrenals, the following procedure was adopted. Two threads were threaded under the upper and lower pole of each adrenal with a minimal amount of dissection so as not to disturb either innervation or circulation of the adrenals. Then after the control observations had been made, gentle pulling of the 4 loose ends of the threads permitted easy lifting of the adrenals, with rapid tying and then tight clamping with a curved hemostat of all the tissues beneath the glands, followed in the first 5 dogs by extirpation of both adrenals in quick succession. Ventricular tachycardia of approximately 220 to 240 per minute was induced electrically with a Grass stimulator, short DC stimuli of minimal intensity being applied to the apex of the left ventricle through 2 fishhook electrodes. Essentially the experiments were conducted as follows. After a control period, ventricular tachycardia ...

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