Cases reported "Hypotension, Orthostatic"

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1/11. Endogenous circulating sympatholytic factor in orthostatic intolerance.

    Sympathotonic orthostatic hypotension (SOH) is an idiopathic syndrome characterized by tachycardia, hypotension, elevated plasma norepinephrine, and symptoms of orthostatic intolerance provoked by assumption of an upright posture. We studied a woman with severe progressive SOH with blood pressure unresponsive to the pressor effects of alpha(1)-adrenergic receptor (AR) agonists. We tested the hypothesis that a circulating factor in this patient interferes with vascular adrenergic neurotransmission. Preincubation of porcine pulmonary artery vessel rings with patient plasma produced a dose-dependent inhibition of vasoconstriction to phenylephrine in vitro, abolished vasoconstriction to direct electrical stimulation, and had no effect on nonadrenergic vasoconstrictive stimuli (endothelin-1), PGF-2alpha (or KCl). Preincubation of vessels with control plasma was devoid of these effects. SOH plasma inhibited the binding of an alpha(1)-selective antagonist radioligand ([(125)I]HEAT) to membrane fractions derived from porcine pulmonary artery vessel rings, rat liver, and cell lines selectively overexpressing human ARs of the alpha(1B) subtype but not other AR subtypes (alpha(1A) and alpha(1D)). We conclude that a factor in SOH plasma can selectively and irreversibly inhibit adrenergic ligand binding to alpha(1B) ARs. We propose that this factor contributes to a novel pathogenesis for SOH in this patient. This patient's syndrome represents a new disease entity, and her plasma may provide a unique tool for probing the selective functions of alpha(1)-ARs.
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2/11. ruscus aculeatus (butcher's broom) as a potential treatment for orthostatic hypotension, with a case report.

    CONTEXT: Chronic orthostatic hypotension (OH) is frequently a severely debilitating disease that affects large groups of the population with autonomic insufficiency--the elderly; patients with diabetes, Parkinson's disease, and chronic fatigue syndrome; and anyone on drugs that affect the autonomic nervous system. Unfortunately, even though more than 60 medications are currently being used to treat OH, none of them is particularly or consistently effective. ruscus aculeatus, a phytotherapeutic agent that is well known in europe, may, however, change this. Its vasoconstrictive and venotonic properties make it ideally suited to treat the pooling of blood in the limbs, lack of venous tone, and lack of neurally mediated vasoconstriction that frequently characterize OH. Although it has never been suggested as a treatment for OH, it already has a long, proven record of use in europe for treating a variety of circulatory disorders. OBJECTIVE: To provide evidence for what appears to be an effective, safe, inexpensive botanical therapy for OH and encourage further studies on the efficacy of ruscus for OH patients. DESIGN: review of OH and therapies currently available for OH and evaluation of the properties of ruscus aculeatus, its mechanism of action, and its suitability as a therapeutic agent for treatment of OH. RESULTS: A review of the many pharmacologic and nonpharmacologic agents for treating OH reveals that all of the drug therapies are disappointing and marginally useful. Although nonpharmacologic management is preferred, in the many cases in which OH becomes debilitating, pharmacologic intervention becomes a last resort. But drug therapy may not always be necessary, because ruscus aculeatus, a phytotherapeutic agent containing ruscogenins and flavonoids, may prove useful for the treatment of OH if denervation is not so advanced that it has compromised receptor activity at the venous wall. ruscus aculeatus is an alpha-adrenergic agonist that causes venous constriction by directly activating postjunctional alpha1- and alpha2-receptors, in turn stimulating the release of noradrenaline at the level of the vascular wall. It also possesses venotonic properties: it reduces venous capacity and pooling of blood in the legs and exerts protective effects on capillaries, the vascular endothelium, and smooth muscle. Its flavonoid content strengthens blood vessels, reduces capillary fragility, and helps maintain healthy circulation. Unlike most of the drug therapies used to treat OH, ruscus aculeatus does not cause supine hypertension. It also appears to do something no other therapy can offer--alleviate the worsening effects of OH in environmentally hot conditions. Finally, it is an extremely safe, inexpensive, over-the-counter botanical medicine. CONCLUSION: With proven phlebotherapeutic properties, including vasoconstrictive action and venotonic properties, ruscus aculeatus shows great promise for ameliorating the symptoms of OH and improving the quality of life for large groups in the population. It clearly deserves to be the object of wider research and study as a treatment for OH.
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3/11. hypersensitivity to noradrenaline in human omental vein but not artery isolated from a patient with idiopathic orthostatic hypotension.

    We investigated the smooth muscle contraction in response to noradrenaline (NA), endothelin-1 (ET) and 5-hydroxytryptamine (5-HT) in the omental artery and vein segments from a 67-year-old woman with idiopathic orthostatic hypotension. The blood vessels were obtained during the abdominal surgery and investigated in vitro. Noradrenaline, endothelin-1 and 5-hydroxytryptamine all induced a contraction in the artery and vein segments. Compared to the literature, the sensitivity to noradrenaline was 10 times higher than expected in the vein. In the artery, the sensitivity to noradrenaline and in both the artery and vein, the sensitivity to endothelin-1 and 5-hydroxytryptamine was similar to that reported in the literature. These results suggest that the patient had developed an isolated hypersensitivity to noradrenaline in the veins, probably due to an impairment of the sympathetic activity.
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4/11. Thyrocervical trunk-external carotid artery bypass for positional cerebral ischemia due to common carotid artery occlusion. Report of three cases.

    Medically refractory positional cerebral ischemia and concomitant orthostatic hypotension associated with chronic common carotid artery (CCA) occlusion are rare. The authors detail their experience with three cases treated exclusively by an extracranial bypass in which the thyrocervical trunk was used as the donor vessel. Postoperatively grafts were patent and symptoms resolved in all three patients, although orthostatic hypotension remained. Postural cerebral ischemia due to CCA occlusion can be treated by extracranial bypass surgery. The thyrocervical trunk is a suitable donor for reconstruction of the external carotid artery in these cases.
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5/11. Successful management of severe aortocaval compression in twin pregnancy.

    In a patient with severe aortocaval compression, simultaneous brachial and femoral blood pressure measurements demonstrated the need for a 30 degrees left-down tilt to avoid significant obstruction of the vessels. When emergency cesarean section became necessary, proper positioning of the patient was readily accomplished.
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6/11. Focal cerebral ischaemia induced by postural change.

    Three middle-aged men with risk factors for vascular disease developed brief, stereotyped hemi-sensory symptoms on sitting or standing. These symptoms occurred in the absence of postural hypotension. On clinical criteria, these episodes were indicative of small vessel (perforator) ischaemia, rather than large vessel disease. This was supported by the absence of any stenosis on duplex scanning of the neck vessels. Two of the patients progressed to develop a fixed deficit. In all 3 patients the outcome was benign, with minimal residual disability.
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7/11. prenalterol in the treatment of orthostatic hypotension in shy-drager syndrome.

    The effects of prenalterol, a selective beta 1-adrenoreceptor agonist, were studied in a patient with the shy-drager syndrome, presenting with incapacitating orthostatic hypotension. The main haemodynamic defect was an impressive postural fall in stroke volume and cardiac output pointing to denervation of the capacitance vessels. prenalterol 4 X 30 mg orally produced a marked increase in supine and standing blood pressure, along with substantial symptomatic improvement. Notable positive chronotropic and inotropic effects were observed. association of fludrocortisone 0.5 mg/day resulted in further haemodynamic and symptomatic improvement, presumably due to plasma volume expansion. Haemodynamically, prenalterol and fludrocortisone resulted in a substantial increase in standing cardiac output, primarily due to the chronotropic effects of prenalterol. In addition to the haemodynamic effects, prenalterol stimulated the renin-aldosterone system and restored the normal diurnal pattern of water and sodium excretion, the latter may have contributed to the improvement of orthostatic tolerance. prenalterol could be a valuable adjunct to the existing treatment schedules of neurogenic orthostatic hypotension.
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8/11. Stroke, orthostatic hypotension, and focal seizures.

    A 75-year-old man had development of left hemiparesis after a cerebral infarction. Nine months later, he was admitted to the hospital after generalized tonic clonic convulsion. In the hospital, he had clonic movement on the left side of the body. Even after acceptable control of orthostatic hypotension, rising from supine to standing position evoked slow waves over the right hemisphere on the EEG tracing. This example of focal seizures with orthostatic hypotension shows that previously compromised cerebral tissue or vessels may be vulnerable to changes in blood pressure. We suggest that convulsive movements associated with hypotension or syncope result from cortical mechanisms rather than brainstem tonic release mechanisms.
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9/11. Idiopathic orthostatic hypotension: circulating noradrenaline and ultrastructure of saphenous vein.

    The present study indicates that patients who can be clinically classified as idiopathic orthostatic hypotensives of the peripheral type are heterogeneous. There is the typical hypoadrenergic type characterized by low levels of circulating noradrenaline, much reduced or absent noradrenaline stores, and correspondingly little or no adrenergic innervation in the saphenous vein, a major capacitance vessel, as confirmed by ultrastructural examination. In one patient of this type, an abnormally high occurrence of mast cells in the blood vessel wall was noted. There also exists a category of individuals of the hyperadrenergic type, analogous to certain diabetics with noradrenergic abnormalities. These patients also are characterized by low levels of circulating noradrenaline, but noradrenaline stores are high; an exaggerated release of neurotransmitter occurs in response to stimuli; the saphenous vein with noradrenergic innervation remains ultrastructurally normal; however, the effector cell response are greatly blunted. In one patient of this type, the smooth muscle cells of the saphenous vein contained excessively high glycogen deposits. Further, it should be anticipated that a variety of intermediate types can be found as exemplified by one patient with variable, low to normal levels of circulating noradrenaline, a sluggish response to release neurotransmitter upon postural challenge, and considerable innervation of saphenous vein but with the majority of axons and terminals undergoing active degeneration.
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10/11. Postural changes in plasma renin activity and responses to vasoactive drugs in a case of shy-drager syndrome.

    A male aged 47 years with gross autonomic insufficiency as part of the shy-drager syndrome is described. He did not sweat normally when warmed, and his circulatory responses to mental arithmetic, the Valsalva manoeuvre, and head-up tilt were abnormal indicating severe sympathetic failure. During head-up tilt there was a rise in plasma renin activity and plasma aldosterone. It is argued that plasma renin activity is not dependent on sympathetic nervous activity and may be mediated by renal baroreceptors. These rises may help sustain the blood pressure in such patients during repeated head-up tilts. Infusions of L-noradrenaline and angiotension produced greater hypertension, and injections of isoprenaline greater hypotension than in controls. Although it is difficult to exclude the possibility that one factor in this may be hypersensitivity of receptors in blood vessel walls, the principal factor is likely to be the absence of those baroreflexes of which the efferent pathways are in the sympathetic nervous system.
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