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At least 19 recordsLinked to original sources
PubMed1977

Use of propranolol in the treatment of idiopathic orthostatic hypotension.

Five patients with idiopathic orthostatic hypotension who had physiologic and biochemical evidence of severe autonomic dysfunction were included in the study. They all exhibited markedly reduced plasma catecholamines and plasma renin activity in both recumbent and upright positions and had marked hypersensitivity to the pressor effects of infused norepinephrine. Treatment with propanolol administered intravenously (1-5 mg) produced increases in supine and upright blood pressure in 4 of the 5 individuals with rises ranging from 11/6 to 22/11 mmHg. Chronic oral administration of propranolol (40-160 mg/day) also elevated the blood pressures of these individuals with increases in the order of 20-35/15-25 mmg being observed. In 1 patient, marked hypertension was induced by propranolol and the drug had to be withdrawn. It otherwise was well tolerated and no important side effects were observed. Treatment has been continued in 3 individuals for 6-13 months with persistence of the pressor effect, although there appears to have been some decrease in the degree of response with time. Hemodynamic measurements in 1 of the patients demonstrated an increase in total peripheral resistance and essentially no change in cardiac output following propranolol therapy. The studies suggest that propranolol is a useful drug in selected patients with severe idiopathic orthostatic hypotension.

Aged↗
PubMed1978

Plasma renin and serum dopamine-beta-hydroxylase during orthostatic hypotension in quadriplegic man.

To determine whether orthostatic hypotension in patients with cervical spinal cord lesions is the result of impaired sympathetic nerve response and/or impaired renin release, serum dopamine-beta-hydroxylase (DbetaH) activity and plasma renin activity (PRA) were examined during passive tilting in 6 quadriplegic patients and in 6 able-bodied control subjects. Serum DbetaH was measured by an isotopic enzymatic method and PRA by radioimmunoassay. Following head-up tilting, quadriplegic subjects demonstrated a prompt, significant decrease in mean arterial pressure (MAP) and increase in heart rate (HR). DbetaH and PRA both increased significantly 15 minutes after tilt. In normal subjects, although HR increased, MAP was unchanged; DbetaH and PRA did not increase significantly during head-up tilt. The finding of increased DbetaH during tilt hypotension in quadriplegic patients provides evidence that reflex sympathetic nerve stimulation persists despite cervical cord transection. Increased PRA may be attributed to decreased renal perfusion pressure and increased sympathetic stimulation during tilt hypotension. These data suggest that orthostatic hypotension in quadriplegia patients cannot be attributed solely to failure of the sympathetic nervous system or the renin-angiotensin system to respond to the stimulus of orthostasis.

Adolescent↗
PubMed1976

Treatment of neurogenic orthostatic hypotension with a monoamine oxidase inhibitor and tyramine.

Six patients with neurogenic orthostatic hypotension were treated with a chemical preparation of tyramine and tranylcypromine ("Parnate"), a monoamine oxidase inhibitor (M.A.O.I.). Four had autonomic failure with no other neurological deficit (idiopathic orthostatic hypotension), and in two patients other neuronal systems were also involved (Shy-Drager syndrome). Previous therapy with fludrocortisone, ephedrine, elastic garments, postural training, and, in one patient, an anti-G suit was unsatisfactory. Tyramine given orally with tranylcypromine produced a moderate rise in blood-pressure which was sustained for 2-4 hours, enabling patients to walk about without symptoms of orthostatic hypotension. Measurement of circulating adrenaline and noradrenaline during therapy suggested that release of noradrenaline caused the pressor response. In three patients there has been a pronounced improvement for 8, 20 and 30 months. In a further patient, therapy has been successful in treating the orthostatic hypotension, although his mobility has been restricted by cerebellar ataxia. In one patient a confusional state developed during treatment and therapy was stopped. The only patient in whom the drugs did not produce a pressor response had orthostatic hypotension with failure of noradrenaline release. It is suggested that the pressor response to a M.A.O.I. and tyramine should be examined in patients with neurogenic orthostatic hypotension and that this treatment should be tried in those who respond.

Administration, Oral↗
PubMed1979

Anaesthetic considerations in idiopathic orthostatic hypotension and the Shy-Drager syndrome.

Orthostatic hypotension due to autonomic failure may occur secondary to systemic disease states (notably diabetes) or as a disease entity in its own right with a variable degree of neurological involvement that has resulted in a confused classification. The diagnosis, classification and treatment of these latter forms of orthostatic hypotension is reviewed. The pathology is in the central and efferent autonomic pathway, resulting in a disordered baro-receptor reflex, postural hypotension, abnormal responses to tilting and the Valsalva manoeuvre, an inappropriately fixed heart rate and other autonomic features. Anaesthesia may be associated with profound hypotension and some of the signs of anaesthesia may be absent. The response to cardiac depressant drugs and reduction of circulating blood volume may be exaggerated due to absence of compensatory mechanisms. The response to vasoactive agents is unpredictable. The importance of preoperative evaluation, monitoring during operation and the careful selection of anaesthetic agents and techniques is discussed.

Adult↗
PubMed1979

Effects of propranolol in a case of orthostatic hypotension.

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.

Blood Pressure↗
PubMed1978

Treatment of idiopathic orthostatic hypotension (Shy-Drager syndrome) with indomethacin.

Four patients with idiopathic orthostatic hypotension (I.O.H.) and one with postural hypotension and diabetes were studied. Plasma-renin activity (P.R.A.) was low and did not rise appropriately with salt restriction and diuretic stimulation. Aldosterone levels were normal and rose with diuretic therapy. Plasma-volume, plasma dopamine beta-hydroxylase, urinary catecholamines, metanephrines, and vanillyl mandelic acid (V.M.A) were normal. Treatment with indomethacin (75-150 mg/day) raised the upright blood-pressure (B.P.) by an average of 20-30 mm Hg diastolic and allowed the four patients with I.O.H. to walk about without orthostatic symptoms but it had no effect in the fifth patient. When indomethacin was discontinued in one patient who had been taking it for 9 months with symptomatic relief, the B.P. fell to pretreatment levels within 48 h. When indomethacin was reinstituted the B.P. rose again. Indomethacin was more effective in these patients than either propranolol or fludrocortisone. There may be an absolute or relative excess of certain vasodepressor prostaglandins in the peripheral vessels which results in pooling of blood and orthostatic hypotension. If this is the case indomethacin might improve the orthostatic symptoms of I.O.H. by its inhibitory effect on prostaglandin synthesis, but its mechanism of action remains to be determined.

Administration, Oral↗
PubMedDate not supplied

[Orthostatic hypotension and obstructive hypertrophic cardiomyopathy (author's transl)].

The authors relate two cases of idiopathic hypertrophic subaortic stenosis detected after orthostatic hypotension with syncope. This type of detection has not been described till now. Relations between idiopathic hypertrophic subaortic stenosis and orthostatic hypotension are debated as well as relation between IHSS and systemic hypertension which has existed previously in the two cases. It seems suitable to call up IHSS systematically before every orthostatic hypotension at least in elderly. Beta-blockers can in such cases considerably improve orthostatic symptoms.

Adrenergic beta-Antagonists↗
PubMed1979

Severe orthostatic hypotension associated with carcinoma of the bronchus.

A patient is described who had severe orthostatic hypotension. An account is given of his treatment with a monoamine oxidase inhibitor and tyramine. At post-mortem, 8 months after the illness began, a small oat cell carcinoma of the bronchus was found. It is suggested that the orthostatic hypotension was a nonmetastatic manifestation of the underlying carcinoma.

Aged↗
PubMed1976

Catecholamine enzymes in the degenerative neurological disease idiopathic orthostatic hypotension.

Discrete brain areas and sympathetic ganglia obtained at autopsy from patients with idiopathic orthostatic hypotension were assayed for tyrosine hydroxylase and dopamine beta-hydroxylase. Dopamine beta-hydroxylase activity was decreased 7.5-fold in sympathetic ganglia, while tyrosine hydroxylase activity was reduced more than 50-fold in the pontine nucleus locus coeruleus. These observations indicate that noradrenergic neurons of both brain and ganglion are affected in idiopathic orthostatic hypotension, but suggest that the central and peripheral biochemical deficits differ.

Aged↗
PubMed1978

[The idiopathic orthostatic hypotension -- Shy-Drager syndrome (author's transl)].

The idiopathic orthostatic hypotension can be characterized as a presenile degenerative process with a liability to attack especially multiple systems. In the course of the disease clinically the autonomic functional failure stands in the beginning. It also determines the serious illness in the later stages, which is associated with an additional variable neurologic syndrome. By means of an own clinically and pathologically examined case it is given a survey of the present knowledge about the disease process. Especially it is declared on the localization of the lesions. Phaemacological tests point to a main disturbance of the preganglionic respectively central part of the sympathetic system. The analysis of the neuropathologically examined cases shows as the most regular finding a neuronal loss in the nucleus intermediolateralis, which certainly is hold responsible for a great part of the functional failure. But it is to assume, that lesions in other structures cooperate in the genesis of the syndrome, which morphologically are not yet recorded.

Autopsy↗
PubMed1979

Mineralocorticoid-induced hypertension in patients with orthostatic hypotension.

The mechanism of recumbent hypertension induced by fludrocortisone was studied in seven patients with orthostatic hypotension. All showed increases in blood pressure in the recumbent and standing positions, and hypertensive levels were achieved on recumbency in four of them. Hypertensive retinopathy developed in two patients and cardiomegaly in one. Initial blood-pressure elevations were associated with sodium retention and plasma-volume expansion. However, with long-term treatment, plasma volume decreased to control levels despite further blood-pressure increases. Treatment did not affect plasma levels of catecholamines but did enhance pressor responsiveness to infused norepinephrine in some subjects. Hemodynamic studies indicated that hypertension in the recumbent position was related to increases in total peripheral-vascular resistance and not to changes in cardiac output. Clinically, hypertension in the recumbent position is an important risk of fludrocortisone treatment in patients with orthostatic hypotension. This unusual model of chronic mineralocorticoid-induced hypertension is not volume dependent but is related to increased peripheral-vascular resistance.

Adult↗
PubMed1979

Decreased sympathetic vasomotor tone in diabetic orthostatic hypotension.

In normals, subcutaneous blood flow in the ankle region, measured by means of the 133Xe washout technique, decreases about 45% when the position of the ankle is changed from cardiac level to 50 cm below the heart. A sympathetic vascular axon reflex is responsible for this flow reduction. A normal response [mean blood-flow reduction, 49% (range, 40 to 64%)] was found in seven diabetics without neuropathy. In nine diabetics with autonomic neuropathy (beat-to-beat variation in heart rate less than or equal to 15 min-1 during hyperventilation), the reduction in blood flow on lowering of the ankle was also normal. A significant deterioration of the response was found in six diabetics with autonomic neuropathy, including orthostatic hypotension, in whom blood flow increased 23% (range, -35 to +77%). Autoregulation of blood flow, i.e., constancy of blood flow in the ankle region on lowering and elevating of the ankle 20 cm below and above cardiac level was intact in the patients with orthostatic hypotension, indicating a normal vascular smooth muscle function. In conclusion, in diabetic patients with orthostatic hypotension, the subcutaneous axon reflex is absent. This may be one of several factors responsible for their orthostatic hypotension.

Adult↗
PubMed1979

Clinical characteristics of imipramine-induced orthostatic hypotension.

The effects of imipramine hydrochloride on blood-pressure were examined in a prospective and a retrospective study. In a prospective study of 44 depressed patients given imipramine in doses to achieve antidepressant plasma-concentrations there was no effect of the drug on lying blood-pressure. When patients then stood up, the drug produced an average fall in systolic pressure of 26 mm Hg (t = 13.6, P less than 0.001) that was consistent over the four weeks of observation. Contrary to expectation, this fall was independent of patients' age, pre-existing heart-disease, or plasma-level of the drug. The best predictor of orthostatic hypotension during treatment was the degree of orthostatic drop in pressure before treatment (r = 0.695, P less than 0.001). In order to establish the clinical significance of this orthostatic drop in pressure, a retrospective study of 148 depressed patients treated with imipramine was conducted. These 148 patients, average age 59 years, received an average dose of 225 mg of imipramine. Almost 20% of them had symptoms usually associated with orthostatic hypotension that were severe enough to interfere with their treatment: over 4% sustained physical injuries. In our experience orthostatic hypotension is the commonest serious cardiovascular side-effect of imipramine.

Adult↗
PubMed1979

Contraindication to the use of ocular phenylephrine in idiopathic orthostatic hypotension.

We studied the effect of topical ocular application of 2.5% phenylephrine ophthalmic solution in patients with idiopathic orthostatic hypotension and in normal subjects. The normal subjects had no pressor effect to the drug. However, the patients with idiopathic orthostatic hypotension, had a marked pressor response. The maximal pressor response in the four patients averaged 44/27 mm Hg. The usual 10% phenylephrine used in practice could have delivered a fourfold greater amount of drug, and presumably would have led to dangerously high blood pressure responses.

Adult↗
PubMed1978

Ultrastructure and biochemistry of sympathetic ganglia in idiopathic orthostatic hypotension.

The role of transsynaptic dysfunction in the pathogenesis of idiopathic orthostatic hypotension (IOH, or idiopathic autonomic insufficiency) was examined microscopically and biochemically in autopsy specimens. Light microscopy of the sympathetic ganglia showed abnormalities in all 4 IOH patients, including focal phagocytosis of neurons, increased numbers of satellite cells, and perivascular lymphocytic infiltrates. Electron microscopy revealed proliferation and hypertrophy of satellite cells and abnormalities in the unmyelinated axons. In contrast, the spinal cord intermediolateral columns, containing the presynaptic neurons, were unremarkable in 1 patient, exhibited only mild gliosis in another, and showed neuron loss and fibrillary gliosis in 2 patients. Postsynaptic dopamine-beta-hydroxylase (DBH) activity was decreased at least fourfold (p less than 0.02) in sympathetic ganglia of patients with IOH, while tyrosine hydroxylase (T-OH) was normal. Ganglion choline acetyltransferase (ChAc) activity, an index of presynaptic function and integrity, was normal in the IOH group. A number of our observations suggest that presynaptic disease is not an absolute requirement for adrenergic abnormalities in IOH. The intermediolateral columns of the spinal cord were histologically normal in 2 of the patients with IOH, and ultrastructural abnormalities in sympathetic ganglia were consistent with primary adrenergic degeneration. In addition, presynaptic ChAc activity was normal in IOH ganglia, whereas postsynaptic DBH activity was depressed. Finally, postsynaptic T-OH activity, which is regulated by transsynaptic mechanisms, was normal in IOH ganglia.

Adrenergic Fibers↗