The effects of adrenergic-blocking agents on the pulmonary circulation in man.

The pulmonary blood vessels are richly inervated with fibres derived from both the sympathetic and parasympathetic nervous systems (Larsell, 1951; Mitchell, 1956) but attempts to demonstrate vasomotricity have yielded conflicting results. If the sympathetic fibres have a pulmonary vasomotor action, it might be anticipated that the administration of an adrenergic-blocking agent would have some demonstrable effect, especially if injected directly into the pulmonary artery. In 1953 Meriel et al. (1953) reported a fall in the pulmonary arterial pressure in normal subjects, in patients with mitral stenosis, and in a single case of primary pulmonary hypertension, following the injection of hydergine into the pulmonary artery through a cardiac catheter. (Hydergine consists of equal parts of the three hydrogenated alkaloids of ergot, dihydroergocornine, dihydroergocryptine, and dihydroergocristine.) They concluded that it exerted a direct action on the vasomotor system of the lungs. Using a similar technique Halmagy et al. (1953b) reported that hydergine had no effect on pulmonary dynamics: they found that dihydroergotamine, when injected into the pulmonary artery, caused a rise in pulmonary arterial systolic pressure and resistance, and concluded that this drug was capable of producing pulmonary vasoconstriction. Similar observations and conclusions regarding dihydroergotamine were reported by Halmagy et al. (1953a). If adrenergic-blocking agents have any effect on the pulmonary circulation, then the manner in which they act has far-reaching implications. It seems important, therefore, to re-examine the action of such an agent, and our purpose is to report the results of seven observations in which hemodynamic measurements were made following the injection of hydergine into the pulmonary artery through a cardiac catheter and four more in which priscol (2-benzyl-2-imidazoline) was injected. In two further observations priscol was administered orally. Material and Methods. The observations were made on thirteen patients selected at random. Nine suffered from mitral stenosis alone and two from mitral stenosis complicated in one by incompetence and in the other by aortic stenosis. One patient suffered from pulmonary heart disease and one from slight pulmonary stenosis. Cardiac catheterization was performed in the usual way and an indwelling needle placed in the brachial artery. Pressures were recorded by means of a capacitance manometer and intra-thoracic pressures referred to a point 5 cm. below the sternal notch. Mean pressures were obtained by electrical filtration. In two cases (155 and 158) the systemic pressure was recorded simultaneously with the pulmonary arterial pressure. Cardiac outputs were estimated by the direct Fick procedure, the expired air being analysed on Haldane's instrument and blood gases by the Van Slyke-Neil manometric method. Vascular resistances were calculated from the following formuke and expressed in c.g.s. units: