These data suggest that, according to the SASSAD score, ABT has beneficial effects in the treatment of AD, although this was not confirmed by the patient-rated assessments. The improvement in observer-rated skin condition suggested by this study needs confirmation in larger trials.

Objective-To determine the effects of a small dose of ft blocker on neurohumoral and cardiopulmonary responses after cardiac transplantation. Background-Cardiac transplant recipients have a reduced exercise capacity and abnormal cardiovascular responses to exercise. The sympathoadrenal response to exercise has been shown to be abnormal with high venous noradrenaline. The effect of ft blockade on these neurohumoral mechanisms has not been defined. Methods-10 non-rejecting cardiac transplant recipients were studied. Patients carried out graded exercise to a symptom limited maximum. Blood samples were taken during exercise. Concentrations of noradrenaline, adrenaline, and atrial natriuretic peptide and plasma renin activity were measured. The next day, the exercise and sampling procedure were repeated after an oral dose of propranolol (40 mg). Results-Patients tolerated exercise poorly after p blockade, which was reflected in the maximum workload reached. Heart rate and blood pressure were significantly higher at rest and during exercise before pl blockade. Although there was no significant difference when resting, mean (SEM) noradrenaline concentrations during peak exercise were higher after p blockade (16.2 (2) v 23-6 (2.9) nmoiIl, p = 0.001). Adrenaline concentrations at peak exercise were also greater after ft blockade

Conscious spontaneously hypertensive rats (SHR), 5--7 wk old, were studied hemodynamically by the direct Fick procedure to determine whether high total peripheral resistance (TPR) coexisted with increased oxygen consumption (QO2) at an early stage of hypertension development. Since under resting conditions cardiac output in SHR was not significantly different from normotensive controls, the elevated arterial pressure and QO2 were associated with increased TPR. Arterial hypoxemia was induced to reduce oxygen availability and to assess whether increased TPR in SHR could be reversed by this procedure. During hypoxemia, normotensive controls (WKY) responded with increased cardiac output and decreased arterial pressure and TPR. In contrast, arterial pressure and cardiac output fell in SHR; and the increased TPR persisted. QO2 fell in hypoxemic SHR demonstrating that the relationship between total body oxygen consumption and cardiac output was abnormal in young SHR, and that increased TPR in SHR was not dependent on resting levels of QO2 or oxygen availability. Although QO2 was elevated in SHR compared to age-matched WKY, this condition was not essential for maintained elevated vascular resistance.

16 patients suffering from a hyperventilation syndrome were treated with metoprolol 2dd 100 mg and an identical placebo in a double-blind, cross-over trial. Before therapy and after metoprolol and placebo therapy a ventilatory response to CO₂ was taken, VC and FEV₁ a hyperventilation provocation test, blood gas values, and the subjective experiences of the patients were documented. The ventilatory response to CO₂ was described in terms of decrease or increase of ventilation: before therapy ventilation decreased in 10 out of 16 patients, after metoprolol ventilation decreased in 3 of 16 patients (p < 0.01). The end tidal Pco₂ increased with a mean of 3.86 mm Hg (p = 0.0005) after metoprolol as compared to placebo. No differences were found in respiratory frequency or depth, base excess, provocation test. It is concluded that the cardioselective beta-blocker metoprolol is a useful drug in the therapy of the hyperventilation syndrome

1. To study the importance of cardiac innervation in the regulation of atrial natriuretic peptide, plasma atrial natriuretic peptide levels were measured during symptom-limited, graded exercise on a cycle ergometer in seven male orthotopic cardiac transplant recipients. 2. Resting plasma atrial natriuretic peptide was significantly higher in the transplant recipients than in two control groups, one matched to the transplant recipients (group I) and the other to the age of the donor heart (group II). 3. The response to exercise of the cardiac transplant recipients was compared with the response of control group II. Mean maximal work load achieved with exercise was around 40% lower in the cardiac transplant recipients. During exercise, plasma atrial natriuretic peptide levels increased in both the cardiac transplant recipients and the control subjects. The increase in plasma atrial natriuretic peptide with exercise was greater in absolute, but less in percentage, terms in transplant recipients than in the control subjects. 4. The increase in mean arterial pressure with exercise was similar in patients and in control subjects; however, heart rate increased in the patients by only 33% compared with a rise of 151% in the control group. 5. These results provide insight into the control of the sodium regulatory hormone atrial natriuretic peptide. First, factors other than a change in heart rate appear of importance in the regulation of atrial natriuretic peptide. Secondly, these findings suggest that cardiac innervation is not of dominant importance in the modulation of atrial natriuretic peptide secretion.