Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven patients with upper airway apnoea during sleep (one with SHY-Drager syndrome) were monitored polygraphically for wakefulness, sleep, and cardiovascular variables. Systemic hypertension and most of the severe arrhythmias recorded during sleep were secondary to repetitive obstructive apnonea and were mediated through the autonomic nervous system. Sleep related elevations of pulmonary arterial pressure were not influenced by atropine or impaired autonomic functions. Upper airway sleep apnoea is sleep related; the type of sleep (REM or NREM) is critical in the appearance of abnormalities. The distinction between two patient subgroups (total sleep dependent and NREM sleep dependent) has haemodynamic, and possibly long-term, implications. Sleep apnoea syndrome should be looked for in pateints with the Shy-Drager syndrome.
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PMID:Sleep apnoea syndrome: states of sleep and autonomic dysfunction. 19 9

Autonomic failure in patients with the Shy-Drager syndrome may produce cardiovascular instability during anaesthesia and surgery. The syndrome is reviewed and the anaesthetic management of a case is described. The choice between general and regional anaesthesia seems to be less important than adequate cardiovascular monitoring and the maintenance of blood pressure with intravenous fluids. Sympathomimetic drugs, if used at all, should be administered in very dilute solutions to avoid hypertension from denervation hypersensitivity. In the postoperative period, symptoms from orthostatic hypotension may be severe and their control requires prolonged postural training, by elevation of the head of the bed, and therapy with 9-alpha-fludrocortisone.
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PMID:Shy-Drager syndrome. A review and a description of the anaesthetic management. 53 23

A patient with autonomic insufficiency and extrapyramidal signs (Shy-Drager syndrome) and sleep apnea syndrome (SAS) underwent hemodynamic studies. In comparison to patients with SAS and intact autonomic reflexes, systemic hypertension was absent and marked sinus arrhythmia during sleep was blunted. Cyclical pulmonary hypertension associated with frequent apneic episodes during sleep persisted, reflecting a minor role of autonomic reflexes in the generation of this abnormality. Autopsy confirmed the Shy-Drager syndrome and multiple areas of degeneration were observed in areas of the CNS outside the medullary respiratory centers, suggesting their importance in the origin of the respiratory abnormalities in SAS.
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PMID:Sleep apnea syndrome in a patient with Shy-Drager syndrome. 62 49

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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PMID:Postural changes in plasma renin activity and responses to vasoactive drugs in a case of Shy-Drager syndrome. 86 77

The effect of xamoterol on the orthostatic hypotension associated with Shy-Drager syndrome was investigated in three patients. Intra-arterial blood pressure was measured during a control period and during treatment with xamoterol, both in a cardiovascular investigation laboratory and for 24 h of unrestricted activity using portable apparatus. Xamoterol lessened the total number of symptomatic episodes of orthostatic hypotension by 67 per cent. Average untreated 24-h intra-arterial blood pressure was 132/78 mmHg; during treatment with xamoterol it rose to 138/90 mmHg. However episodes of severe hypertension (defined as a systolic intra-arterial blood pressure above 200 mmHg) were more frequent with xamoterol. Although xamoterol attenuated orthostatic hypotension, careful monitoring of ambulatory blood pressure may be necessary, particularly at the start of treatment, because of the development of severe supine hypertension. Intravenous test doses of xamoterol did not predict either the attenuation of orthostatic hypotension or the development of supine hypertension in all patients.
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PMID:Xamoterol in the treatment of orthostatic hypotension associated with multiple system atrophy (Shy-Drager syndrome). 197 24

Ambulatory blood pressure monitoring can determine the average blood pressure level and the short- and long-term blood pressure variability (circadian rhythm). The circadian blood pressure rhythm appears to be mediated mainly by the circadian rhythm of the sympathetic tone which is linked to changes in physical and mental activity, e.g. the waking-sleeping cycle. A statistically significant circadian blood pressure rhythm was observed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, in patients with Cushing's syndrome, under glucocorticoid treatment, or with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, spinal cord injury, brainstem lesions, diabetic neuropathy, uremic neuropathy, etc), chronic renal failure, eclampsia, malignant hypertension, sleep apnea syndrome or systemic atherosclerosis, the normal circadian blood pressure rhythm appears to be eliminated or reversed, while in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, diabetes insipidus, acromegaly, hyperparathyroidism or hyperprolactinemia, the nocturnal blood pressure fall has been observed as in normal subjects. The alteration in the circadian blood pressure rhythm was observed with different pathophysiological conditions, although no specific pattern was observed for any condition. A disturbance in any part of the hierarchy of factors that regulate the circadian rhythm of sympathetic neural tone seems to disturb the circadian blood pressure rhythm. We conclude that ambulatory blood pressure monitoring is not critically important in the diagnosis of secondary hypertension although it does help in screening for secondary hypertension.
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PMID:Does ambulatory blood pressure monitoring improve the diagnosis of secondary hypertension? 208 1

The daily variation in blood pressure (circadian blood pressure rhythm) is characterized by a nocturnal fall and a diurnal rise. The circadian blood pressure rhythm seems to be mediated mainly by the circadian rhythm of sympathetic tone, linked to changes in physical and mental activities, e.g. the waking-sleeping cycle. Statistically significant circadian blood pressure rhythms have been confirmed in approximately 80% of mild to moderate essential hypertensive patients as well as in normal subjects. However, the normal pattern of circadian blood pressure rhythm is reversed in elderly people and in those with Cushing's syndrome, those undergoing glucocorticoid treatment, and those with hyperthyroidism, central and/or peripheral autonomic dysfunction (Shy-Drager syndrome, tetraplegia, diabetic or uremic neuropathy, etc), chronic renal failure, renal or cardiac transplantation, congestive heart failure, eclampsia, sleep apnea syndrome, malignant hypertension, systemic atherosclerosis and accelerated hypertensive organ damage. However, in those with primary aldosteronism, renovascular hypertension, pheochromocytoma without paroxysmal hypertension, or those with cardiac pacing, a nocturnal blood pressure fall is ordinarily observed. It may be that a fall in cardiac output rather than in peripheral resistance may be mainly responsible for the nocturnal fall in blood pressure. It also seems that a nocturnal heart rate fall is not responsible for it, since the nocturnal blood pressure fall remained unchanged in patients undergoing cardiac pacing and was disturbed in patients with Cushing's syndrome or hyperthyroidism in whom the circadian heart rate rhythm remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian blood pressure variations under different pathophysiological conditions. 209 80

Endothelin (5 nmol/kg, i.v.) caused a transient hypotension followed by a lasting hypertension in rats. However, an abrupt fall in the blood pressure was observed in most rats 6 to 30 min after the injection of endothelin and sudden death followed with lethality noted over 60 min. An abnormal electrocardiogram (ECG) (ventricular arrhythmias) was observed in rats injected with endothelin. Endothelin (i.v.) also caused sudden death in mice. Pretreatment (5 or 60 min) with specific PAF antagonists, CV-6209 (0.1-3 mg/kg, i.v.) and WEB 2086 (30 mg/kg, p.o.), and a calcium channel blocker, diltiazem (60 mg/kg, p.o.) prevented death and attenuated the ECG changes induced by endothelin, but CV-6209 did not prevent the blood pressure changes induced by endothelin. CV-6209 (0.5-3 mg/kg, i.v.), WEB 2086, diltiazem and dexamethasone (5 mg/kg, i.v.) protected mice against the death induced by endothelin. On the other hand, aspirin (cyclooxygenase inhibitor, 100 mg/kg, p.o.) did not protect mice from the death. Thus, endothelin is a highly toxic peptide with cardiotoxic effects, and PAF may be involved in the pathogenesis of the sudden death.
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PMID:Endothelin-induced sudden death and the possible involvement of platelet activating factor (PAF). 268 21

A 43-year-old male with "pure" progressive autonomic failure ("pure" PAF) was admitted to our hospital in June 1988, with a chief complaint of recent syncopal attacks while standing. Since the age of 35. He has noticed dyshidrosis on his left side. The family history was negative. Neurological examination showed dyshidrosis on his left side and profound orthostatic hypertension. No other neurological abnormalities were noted. Autonomic function tests revealed sympathetic and parasympathetic dysfunction as follows: Adrenaline administered subcutaneously gave a hyperactive pressor response from 136/82 mmHg to 190/116 mmHg with the pulse increasing from 54 to 150 beats per min. Hidrosis was observed on the right side of the body in response to heat. However, it was observed over the whole body in response to pilocarpine. In the studies of pupillary response to instillation of 1.25% epinephrine, both pupils were unchanged in diameter; after 5.0% tyramine, both pupils were dilated from 3.5 mm to 5.0; and after 2.5% methacholine, the right and left pupils, each originally 4.5mm were constricted to 3.5 mm and 4.0 mm, respectively. From the above data, this case was diagnosed as "pure" PAF. 133Xe inhalation method. The mean regional CBF (F1) values were reduced from 91 to 53 ml/100 g brain/min by postural change from supine to sitting position, associated with a decrease in mean arterial blood pressure (MABP) of 28 mmHg (from 103 to 75 mmHg). This result shows the impairment of CBF autoregulation in this patient. This case adds further evidence to the hypothesis that the autonomic nervous system plays a role in CBF autoregulation.
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PMID:[A case of "pure" progressive autonomic failure with impairment of cerebral blood flow autoregulation]. 269 14

Cerebral ischemia and ischemia-reperfusion induced cerebral injury results in the accumulation of free fatty acids and diacylglycerols as a result of increased activity of phospholipases A and C. We have evaluated the incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomes, the effect of cerebral ischemia on 14C incorporation, and the effect of a PAF antagonist (BN 52021) on cerebral blood flow, free fatty acids, diacylglycerols, and polyphosphoinositides. Peak incorporation of 14C arachidonic acid into the whole brain and synaptoneurosomal fractions occurred 30 minutes following intraventricular injection. Peak incorporation into cerebellar synaptoneurosomal fractions was at 60 minutes following intraventricular injection. Turnover in phospholipid pools was similar in the whole brain and synaptoneurosomes (PI greater than PC greater than PE). Considering phosphatidylinositol content in the gerbil brain, the specific activity of 14C arachidonic acid was 22 times greater in PI than PC. Five minutes of bilateral carotid artery ligation resulted in decreased phosphatidylinositol and polyphosphoinositols. Bilateral carotid artery ligation resulted in systemic arterial hypertension, complete forebrain ischemia (CBF less than 7 ml/100 gm/min) and a 20% to 50% reduction in midbrain CBF. Reperfusion resulted in cerebral reactive hyperemia and systemic hypotension. BN 52021 inhibited the maturation of ischemia-reperfusion induced cerebral injury. Cerebral blood flow was improved. Free fatty acids were decreased, suggesting inhibition of phospholipase A activity. Decreased DAG pools with increased PIP2 pools suggest a possible coinhibition of phospholipase C.
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PMID:Arachidonic acid metabolism and cerebral blood flow in the normal, ischemic, and reperfused gerbil brain. Inhibition of ischemia-reperfusion-induced cerebral injury by a platelet-activating factor antagonist (BN 52021). 277 4


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