Steroid secretion was studied in conscious dogs before and during 4 days of Na depletion. A threefold increase in aldosterone secretion occurred but corticosterone output was unchanged. Plasma renin was markedly elevated. Plasma Na and K concentrations were unchanged until the 4th day of Na depletion at which time plasma Na was decreased and plasma K was elevated. The Na content of the adrenal cortex expressed as fat-free tissue solids was decreased. It seems likely that the adrenocortical Na loss was extracellular; adrenocortical K content was unaltered. It is suggested that the normal rate of corticosterone secretion during Na depletion is maintained by a negative corticosteroid feedback mechanism, since corticosterone output was consistently increased in Na-depleted hypophysectomized dogs. Aldosterone secretion was three times as great in the presence as in the absence of the anterior pituitary during Na depletion. It is concluded that increased activity of the renin-angiotensin system is the primary mechanism leading to hyperaldosteronism during Na depletion and that the adenohypophysis plays an important supportive role.

The central and peripheral vascular haemodynamic effects of glucagon were studied in 29 and peripheral haemodynamic effects of glucagon in patients with organic heart disease. Patients and MethodsA total of 29 patients was studied; they were divided into the following groups: (i) the acute phase of myocardial infarction (8 patients); (2) chronic rheumatic heart disease (II patients); (3) a selection of I0 patients chosen for measurement of forearm and calf blood flow. As the technique varied for each group the methods and results will be described for each in turn.

Frusemide is a well-established diuretic (Vorburger, 1964;McKenzie, Fairley, and Baird, 1966;Kirkendall and Stein, 1968), and a mild hypotensive when given in a dosage of over 120 mg. daily (Davidov, Kakaviatos, and Finnerty, 1967). It is commonly used in the treatment of acute pulmonary oedema with beneficial results (Stason et al., 1966;Peltola, 1965;Biagi and Bapat, 1967 Though some work has been done-on the systemic haemodynamic effects of frusemide (International Furosemide Symposium, Bad Homburg, 1963), little or no information is available on its effect on left atrial pressure and pulmonary haemodynamics in patients either with normal or raised left atrial pressure. It was because of this paucity of information in association with its obvious clinical benefit in patients with acute pulmonary oedema that this study was instituted to investigate its haemodynamic effects in these 2 groups of patients. PATIENTS AND METHODSA total of 23 patients was studied, and for convenience the patients were divided into 2 groups. In the first group were 8 patients whose mean left atrial pressure was under 10 mm. Hg. In the second group 15 patients had mitral valve disease with a mean left atrial pressure above 10 mm. Hg, six of them had episodes of paroxysmal nocturnal dyspnoea, and all experienced dyspnoea on exertion.All patients had right heart catheterization and either Received May 9, 1969. * In receipt of a Research Award from the British Heart Foundation. 711 a brachial artery needle or retrograde aortic catheter inserted. In addition, those with valvular heart disease had left atrial catheterization performed using a modified Brockenbrough needle with a blunt-ended stylette. Cardiac outputs were measured by injecting indocyanine green dye (2-5 mg.) into the pulmonary artery with constant arterial withdrawal through a Gilford densitometer, and the dye curve was recorded on either a Sanborn photographic recorder or an ultraviolet recorder. Pressures in the pulmonary artery, brachial artery or central aorta, and the left atrium were measured at rest under mild sedation using a Sanborn pressure transducer (Model 267B) coupled to a Sanborn photographic recorder. The reference point for all pressure determinations was 5 cm. below the sternal angle and a simultaneous electrocardiogram was taken with all pressure measurements. One or two control cardiac outputs were determined and their average taken. Frusemide was injected directly into the pulmonary artery through the catheter in a dose of 40 mg. over a two-minute period, and the above parameters were measured 15 minutes and 45 minutes later.The following values were derived from the results: Cardiac output (ml./sec.) x 1332Central blood volume (ml.) = Appearance time of dye (sec.) x cardiac output (ml./sec.)Pressure-time index (mm. Hg sec./min.) = Ejection time (sec.) x mean ejection pressure (mm. Hg) x heart rate (beats/min.)

There is little doubt concerning the efficacy of lignocaine (Xylocaine) in the treatment of many cardiac arrhythmias, particularly during cardiac catheterization (Southworth et al., 1950), during intubation and induction of anaesthesia and cardiac surgery (Weiss, 1960), and after myocardial infarction (Lown et al., 1967;Jewitt et al., 1968;Spracklen et al., 1968). In spite of the apparent value of the drug there is little information on its haemodynamic effects, and this communication is concerned with evaluating its effect in small doses in man and much larger doses in dogs. This investigation was done to determine whether a continuous infusion of lignocaine could be used in all patients after myocardial infarction to suppress the common ventricular ectopic beats, and possibly act as a prophylactic measure to prevent arrhythmias causing further myocardial deterioration. Lown et al. (1967) expressed the opinion that antiarrhythmic drugs might jeopardize survival after myocardial infarction by reducing myocardial contractile force. Methods PatientsFour patients (weight 40.6-79.8 kg.) undergoing cardiac catheterization under light barbiturate anaesthesia with a view to possible surgery were investigated. Measurements were taken before and after an intravenous dose of lignocaine (1 mg./ kg.) given over a two-minute period, and 10, 20, 30, and 60 minutes after starting a lignocaine infusion given with a homemade constant infusion pump (1 mg./min. in a volume of 2 ml. of isotonic saline; total dose was approximately 120 mg. of lignocaine). Conventional catheters were used and transseptal left atrial catheterization was performed with a modified Brockenbrough needle; in one instance left ventricular pressure was measured with a transseptal catheter through the mitral valve (the maximum rate of rise of left ventricular pressure, dp/dt, was measured and taken as the average of five values determined by a tangent drawn on the steepest part of the pressure tracing ; the rate at which ventricular pressure is developed reflects a fundamental property of contracting myocardium and may be used to study myocardial contractility (Gleason and Braunwald, 1962) An intravenous infusion of lignocaine (10-13.5 mg./min.) was given with a constant infusion pump, and cardiac output, central aortic pressure, and the electrocardiogram were recorded after 10, 20, and 30 minutes of infusion. After a rest period these measurements were recorded before and after a rapid intravenous injection of 200 and 400 mg. of lignocaine (given as a 2 % solution), and in one instance after 500 mg.