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.)

Objective-To determine whether percutaneous transluminal coronary angioplasty may be safely performed in cardiology centres in the United Kingdom without immediate on site cardiac surgical cover for complications arising at angioplasty.Design-Retrospective review of coronary angioplasties and complications in a hospital without on site cardiac surgical cover.Setting

1 The acute haemodynamic effects of i.v. pinacidil 0.2 mg kg-' infused over 8 min were studied in 10 normotensive patients undergoing cardiac catheterisation. 2 Mean arterial pressure fell from 94 ± 3 mmHg (mean ± s.e. mean) before infusion to 74 ± 3 mmHg at 10 min after commen--ng infusion (P ' 0.001) and during this time heart rate increased from 75 ± 4 to 106 ± 7 beats min-' (P < 0.001). Significant changes were recorded until the end of the observation period (70 min after commencing infusion). 3 Cardiac index increased from 3.2 ± 0.2 to 4.0 0.2 1 min-' m-2 (p < 0.001) and systemic vascular resistance fell from 16 ± 1 to 10 1 units (P < 0.001) at 10 min after commencing infusion. By the end of the observation period, the values had returned to pre-infusion levels. 4 Only small changes in pulmonary haemodynamics were observed. 5 These results indicate that pinacidil acts as a peripheral arteriolar vasodilator, and as such may have a role in the treatment of arterial hypertension and of cardiac failure.