Postural Syncope Research Articles

Autoimmune preganglionic sympathectomy induced by acetylcholinesterase antibodies.

Systemic injection of monoclonal antibodies to neural acetylcholinesterase in adult rats caused a syndrome with permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensued. In sympathetic ganglia, acetylcholinesterase activity disappeared from neuropil but not from nerve cell bodies. Choline acetyltransferase activity and ultrastructurally defined synapses were also lost. Electrical stimulation of presynaptic fibers to the superior cervical ganglion ceased to evoke end-organ responses. On the other hand, direct ganglionic stimulation remained effective, and the postganglionic adrenergic system appeared intact. Motor performance and the choline acetyltransferase content of skeletal muscle were preserved, as was parasympathetic (vagal) function. This model of selective cholinergic autoimmunity represents another tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.

Hypotension With Postural Syncope Secondary to the Combination of Chlorpromazine and Captopril

A 49-year-old man with severe hypertension and chronic schizophrenia developed marked hypotension with postural syncope following therapy with the combination of chlorpromazine and captopril. Previously, the patient's blood pressure (BP) had been poorly controlled on a regimen of chlorpromazine and hydrochlorothiazide, nadolol, and prazosin. The supine and standing BP and 24-hour ambulatory BP were subsequently studied while the patient was maintained on chlorpromazine and captopril, chlorpromazine alone, and on no therapy. Chlorpromazine alone caused a moderate reduction in supine and standing BP with a reversal of the circadian BP profile. The combination of chlorpromazine and small doses of captopril (12.5 mg/d) induced a reduction in supine BP of 84/32 mm Hg compared with chlorpromazine alone and exaggerated the postural hypotension. Hormonal investigation demonstrated low baseline renin activity that increased during therapy with captopril and a physiologic catecholamine response to change in posture. These data demonstrate that there is a synergism between captopril and chlorpromazine that may result in marked, symptomatic hypotension that is probably unrelated to the baseline level of plasma renin activity or catecholamines.

Hypotension with postural syncope secondary to the combination of chlorpromazine and captopril

Hypotension with postural syncope secondary to the combination of chlorpromazine and captopril

Postural syncope and trigeminal neuralgia relieved by percutaneous rhizotomy with glycerol

Postural syncope and trigeminal neuralgia relieved by percutaneous rhizotomy with glycerol

Orthostatic hypotension in familial amyloid polyneuropathy: treatment with DL-threo-3,4-dihydroxyphenylserine.

We measured plasma norepinephrine levels in patients with familial amyloid polyneuropathy. Patients with orthostatic hypotension had low basal plasma norepinephrine levels, which did not increase after postural change. On the basis of biochemical findings that suggest depletion of peripheral norepinephrine, DL-threo-3,4-dihydroxyphenylserine, an immediate precursor of norepinephrine, was given orally. Six hundred mg of this drug induced substantial and sustained elevation of blood pressure for several hours, and plasma norepinephrine content increased. Daily administration for 4 weeks improved postural dizziness and syncope, and daily activity increased.

Inhibition of propranolol metabolism by chlorpromazine.

The effects of chlorpromazine 50 mg 8‐hourly on the disposition and effectiveness of propranolol have been investigated in 5 subjects. Propranolol was given orally in a dose of 80 mg 8‐hourly and after 3 days H3‐propranolol was injected intravenously. Both native and H3‐drug were measured in serial blood samples, allowing calculation of intrinsic (oral) clearance and liver blood flow as well as the usual kinetic parameters. The study was repeated after 3 or 4 days of chlorpromazine treatment. Chlorpromazine consistently produced a reduction in intrinsic (oral) clearance from 4.30 ± 0.51 to 2.94 ± 0.16 (p < 0.01), indicative of inhibition of propranolol metabolism. This was associated in an increase in bioavailability from 25 ± 3 to 32 ± 4% (p < 0.005). As would be expected with a highly extracted drug, the change in systemic (intravenous) clearance was much less and was not significant. There were no changes in liver blood flow, volume of distribution, t½, or plasma binding of propranolol. Propranolol efficacy was determined in 3 subjects. In 2 of these plasma levels of propranolol were increased by chlorpromazine at the time of study and resulted in increased isoproterenol antagonism and lowered plasma renin activity. In the third subject plasma propranolol levels were only slightly elevated and no clear pharmacodynamic changes were detected. A sixth subject experienced postural hypotension and syncope following the first dose of chlorpromazine. It was unclear whether this was due to chlorpromazine alone or to an interaction with propranolol. We conclude that chlorpromazine can inhibit the metabolism of propranolol in man, thereby increasing propranolol efficacy.

Comparison of clonidine and methyldopa on blood pressure and side effects in hypertensive patients

Clonidine hydrochloride (Catapres) represents a new type of antihypertensive agent which acts to reduce blood pressure by central inhibition of sympathetic vasomotor and cardioexcitatory stimuli. 1,2 We have previously demonstrated its antihypertensive effectiveness particularly when combined with a diuretic. 3 The drug has been shown to have long-term effectiveness in the treatment of severe hypertension and sufficient potency to replace guanethidine. Sedation, constipation, and dry mouth are its chief side effects; they tend to decrease with the passage of time and are less objectionable than the fatigue and postural syncope frequently seen with guanethidine. 4 Clonidine is also useful in smaller doses in the treatment of less severe forms of hypertension, where other antihypertensive drugs such as alpha methyldopa may also be effective. The purpose of the present study is to compare these two drugs at a fixed dosage, both concerning their hypotensive effectiveness in patients with moderately severe hypertension and also concerning side effects produced by each agent when the blood pressure is lowered to a comparable degree.

Comparison of the reflex reactivity of skin and muscle veins in the human forearm.

To determine the relative participation of skin and muscle capacitance beds of the forearm in venomotor reflexes, epinephrine iontophoresis was combined with forearm plethysmography so that the volume of muscle veins could be estimated simultaneously with the volume of cutaneous veins, at a constant venous pressure. With this technique not only are the cutaneous veins markedly constricted but they also are prevented from filling since skin blood flow is abolished. In 10 normal subjects, the venous volume in the elevated control forearm at a congesting pressure of 30 mm Hg (VV[30]) was 3.16 +/-0.30 SEM cc/100 cc, while in the iontophoresed arm it was 2.54 +/-0.31 cc/100 cc. Thus the forearm cutaneous VV[30] was 1.62 cc/100 cc. With a deep breath, ice to the forehead, and leg exercise, and cutaneous VV[30] decreased 19.8% (P < 0.01), 36.6% (P < 0.01), and 32.6% (P < 0.02), respectively, whereas the muscle VV[30] was not altered significantly. Similar results were observed using the isolated forearm technique and a deep muscle vein. The infusion of epinephrine intra-arterially did not decrease reflex venomotor reactivity until cutaneous blood flow was completely suppressed, indicating that the inability of the veins to react in the iontophoresed arm was not the result of epinephrine diffusion into the muscle bed. Thus, these results indicate that, in the forearm, only cutaneous veins participate in venomotor reflexes. Further, since the forearm is principally composed of skeletal muscle and the hand skin, an explanation is provided for the observation that veins of the forearm, studied as a whole, appear less reactive to stimuli than veins of the hand. An explanation also is provided for fainting which occurs during motionless standing despite intense venoconstriction, thereby emphasizing the importance of the skeletal muscle pump in the legs in preventing postural syncope.

Comparison of footboard and saddle supports for orthostatic tests on a tilt table.

ArticleComparison of footboard and saddle supports for orthostatic tests on a tilt table.R H Murray, J A Bowers, and E R GoltraR H Murray, J A Bowers, and E R GoltraPublished Online:01 Jul 1966https://doi.org/10.1152/jappl.1966.21.4.1409MoreSectionsPDF (654 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByFeatures of vascular regulation of students – future specialists in physical education and sports of different sports specializations with different body lengths28 June 2021 | Health, sport, rehabilitation, Vol. 7, No. 2Cardiac performance is influenced by rotational changes of position in the transversal plane, both in the horizontal and in the 60̊ head-up postures26 April 2018 | Clinical Physiology and Functional Imaging, Vol. 38, No. 6Relation of Postural Vasovagal Syncope to Splanchnic Hypervolemia in AdolescentsCirculation, Vol. 110, No. 17Assessment of Cardiovascular Regulation during Head-up Tilt and Suspension in SwimmersMedicine & Science in Sports & Exercise, Vol. 36, No. 1Usefulness of tilt test–induced patterns of heart rate and blood pressure using a two-stage protocol with glyceryl trinitrate provocation in patients with syncope of unknown originThe American Journal of Cardiology, Vol. 84, No. 6Head-up suspension in humans: effects on sympathetic vasomotor activity and cardiovascular responsesA. S. M. Shamsuzzaman, Y. Sugiyama, A. Kamiya, Q. Fu, and T. Mano1 May 1998 | Journal of Applied Physiology, Vol. 84, No. 5Head-up tilt table test: how far and how long?Clinical Autonomic Research, Vol. 6, No. 6Combined head-up tilt and lower body suction: A test of orthostatic toleranceClinical Autonomic Research, Vol. 4, No. 1-2Methodology of head-up tilt testing in patients with unexplained syncopeJournal of the American College of Cardiology, Vol. 17, No. 1The Measurement of Orthostatic Tolerance2 July 2016 | Human Factors: The Journal of the Human Factors and Ergonomics Society, Vol. 14, No. 4Cardiovascular Effects of Cold Pressor Tests, 40° Head-up Tilt, and Smoking on Smokers and Non-smokersDiseases of the Chest, Vol. 56, No. 4 More from this issue > Volume 21Issue 4July 1966Pages 1409-11 https://doi.org/10.1152/jappl.1966.21.4.1409PubMed5916687History Published online 1 July 1966 Published in print 1 July 1966 Metrics

PUBERTAL HYPOTHYROIDISM. LACK OF GROWTH RESPONSE AFTER THYROID REPLACEMENT.

Thyroidal failure at puberty produces a syndrome with clinical manifestations intermediate between those of cretinism and adult myxedema. In addition to the symptoms of generalized hypometabolism, there are disturbed gonadal maturation, growth failure, and mental retardation, in variable degrees, dependent on the time of onset and extent of thyroprivia. Although it is stated broadly in textbooks that thyroid hormone replacement will reverse all of the hypothyroid changes, there are few reports which document the effect of therapy on growth. The observation of a patient with pubertal hypothyroidism, growth failure, and nonunited epiphyses, and who had no linear growth but epiphyseal fusion after prolonged thyroid medication, prompts this report. Report of a Case This patient, a 22-year-old white man, was admitted to US Naval Hospital, Oakland, Calif, on Jan 22, 1961, following a hypotensive episode. On the day of admission he experienced nausea, vomiting, and periumbilical pain followed by postural syncope.

Acute Reduction in Intracranial Pressure as a Mechanism of Postural Syncope

Acute Reduction in Intracranial Pressure as a Mechanism of Postural Syncope

Acute reduction in intracranial pressure as a mechanism of postural syncope in a patient with postoperative lumbar meningocele.

Acute reduction in intracranial pressure as a mechanism of postural syncope in a patient with postoperative lumbar meningocele.

Cerebral blood flow, cardiac output, cardiac work, mean arterial pressure and right heart pressure during postural syncope

Cerebral blood flow, cardiac output, cardiac work, mean arterial pressure and right heart pressure during postural syncope

Orthostatic hypotension, anhidrosis, and impotence.

Anhidrosis and impotence occur frequently with idiopathic orthostatic hypotension. Two new cases of this syndrome, which occurs chiefly in males over 40 years of age, are herewith described. Postural vertigo and/or syncope, weakness, and anhidrosis or hypohidrosis are common symptoms, and a marked fall in systolic and diastolic blood pressure is noted when the patients stand. The pathologic physiology of the syndrome is discussed and various forms of therapy, none of them especially satisfactory, are reviewed.

Observations of Nitrite-Induced Postural Syncope in Patients with Mental Disease

Summary and conclusionsIn patients with mental or emotional disorders, increased activity of vasomotor mechanisms responsive to postural change may occur; this is observed irrespective of diagnosis. In some psychotic patients disturbances in mental content and mood, consisting of intensification of pre-existing psychotic manifestations, occurred at times when it may be assumed that cerebral blood flow was diminished. Observations suggest that lobotomy causes no distinctive change in postural vasomotor reactivity when time for complete healing is allowed.