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Continuous intra-arterial blood pressure measurement and electrocardiograms were obtained in two ambulatory patients with orthostatic hypotension due to autonomic dysfunction. Systolic and diastolic arterial pressure presented marked variations which took place mainly during the day and were related to several physical activities; however, marked falls in blood pressure were also observed during sleep and at the moment of arousal. A peak incidence of hypotensive events was found in the afternoon, mainly in the hours following the afternoon meal. Recording was repeated after 3 weeks of treatment with propranolol, 40 mg t.i.d. In patient 1, beta blockade drastically reduced the number and severity of hypotensive episodes, while propranolol failed to control blood pressure in patient 2, who experienced a higher number of hypotensive events during treatment. Findings of this study may be relevant to the management of patients with orthostatic hypotension and should contribute to a more accurate characterization of blood pressure profile in autonomic dysfunction.

In a hypertensive patient with orthostatic hypotension, the changes in several haemodynamic indices with respect to posture were evaluated. In the upright position, systemic blood pressure was reduced as compared with the supine position, and peripheral vasodilation was present, as shown by an increase in Jantsch's index of the impedance plethysmographic tracings. Systolic time intervals remained unchanged with changes in posture. Propranolol 10 mg intravenously brought the response to normal. In fact, after beta-blockade in the standing position the blood pressure remained unchanged and normal peripheral vasoconstriction was observed. Similar results were seen during atrial pacing at a constant heart rate of 130 beats/minute. In this patient, propranolol appears to normalise the response to the posture change, by restoring normal vasoconstriction in the upright position.

A double-blind, cross-over study was designed to evaluate the effects of L-carnitine in patients with peripheral vascular disease. After drug washout, 20 patients were randomly assigned to receive placebo or L-carnitine (2 g bid, orally) for a period of 3 weeks and were then crossed over to the other treatment for an additional 3 weeks. The effect on walking distance at the end of each treatment period was measured by treadmill test. Absolute walking distance rose from 174 +/- 63 m with placebo to 306 +/- 122 m (p less than .01) with carnitine. Biopsy of the ischemic muscle, carried out before and after 15 days of L-carnitine administration in four additional patients, showed that treatment significantly increased total carnitine levels. An additional goal of this study was to ascertain the effects of L-carnitine on the metabolic changes induced by exercise in the affected limb. In six patients under control conditions, arterial and popliteal venous lactate and pyruvate concentrations were determined at rest, when the maximal walking distance was reached, and 5 min after the walking test. Twenty-four hours later, L-carnitine was administered intravenously (3 g as a bolus followed by an infusion of 2 mg/kg/min for 30 min) and metabolic assessments were repeated. Five minutes after the walking test, popliteal venous lactate concentration increased by 107 +/- 16% before treatment and by only 54 +/- 32% (p less than .01) after carnitine. Furthermore, carnitine induced a more rapid recovery to the resting value of the lactate/pyruvate ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

In two patients with orthostatic hypotension, due to autonomic dysfunction, hemodynamic changes induced by the assumption of erect position have been evaluated before and during chronic propranolol treatment. Under control conditions, the change in posture induced in Patient 1 a fall in systolic and diastolic blood pressure by 51.4 and 30.7%, respectively. Cardiac output was reduced by 26.8% and systemic vascular resistance by 23.3%. During propranolol treatment, systolic pressure decreased only by 28% and diastolic pressure by 7.7%. The decline in systemic vascular resistance on standing was abolished, while the reduction in cardiac output remained unmodified. In Patient 2, symptoms of orthostatic hypotension were related to marked decrease in systolic blood pressure, the diastolic pressure remaining unchanged. Moreover, systemic vascular resistance increased and, thus, orthostatic hypotension was exclusively dependent upon the severe fall in cardiac output on standing. As a consequence, propranolol failed to control orthostatic hypotension in this patient. These data suggest that when orthostatic hypotension is secondary to failure in peripheral vasoconstriction, propranolol may act beneficially. When it is secondary to a fall in cardiac output, beta-blockade is ineffective.