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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

4 patients with hypertensive crisis (glomerulonephritis [n = 2], phaeochromocytoma [n = 1], reno-vascular hypertension [n = 1] combined with encephalopathy, showed a normalisation of blood-pressure up to 18 days during angiotensin-II-blockade with saralasin. Prior, blood pressure was treated insufficiently by intravenous diazoxide and Na-nitroprusside. Increased plasma-renin-activity and plasma levels of catecholamines pointed to an activation of the renin-angiotensin- and sympathico-adrenergic system. A trial of therapy with saralasin--especially, if blood-pressure response to diazoxide and sodium-nitroprusside is insufficient--could be indicated. Side-effects like pressor-reactions are excluded by very low priming doses (0,1 microgram/kg/min); rebound-hypertension at the end of the therapy is avoided by an overlapping therapy with renin suppressing drugs (beta-receptor blockers, clonidine, guanfacinum).
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PMID:[Saralasin in resistant hypertensive crisis (author's transl)]. 3 82

From the surgical point of view is reported on the therapy of the portal hypertension by operations of anastomoses decreasing the pressure. Here the treatment of the haemorrhage of the oesophageal varices dangerous to life is in the first place. The porto-caval shunt is justified and successful in this emergency situation, since it has the decisive advantages of a short time of operation and an optimal release of pressure. Obstructive operations are indicated only in exceptional cases. Issuing from the haemodynamic criteria and from the moment of haemorrhage, the indication to the typical shunt operations is explained. Hereby it is established that the surgery of portal vessels is still considerably burdened by the postoperative encephalopathy. The modern anastomotic operations are directed to its prevention. Finally the author adopts a definite attitude to the peculiarities of the hypertension of the portal vein in children and it is in short referred to the operative treatment of the therapy-resistent ascites as well as of the hypersplenism.
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PMID:[Surgical treatment of portal hypertension]. 30 Sep 52

The authors reports the results of 171 cases of portal systemic by pass operations out of a total of 200 cases operated on between 1968 and 1974. These 171 patients all presented with a syndrome of portal hypertension with oesophageal varices and all had previously bled. Their age lay in 70 p. cent of cases between 40 and 60 years and the cause of hypertension was in 96 p. cent of cases an intra-hepatic block. 41 p. cent were included in the risk group A according to Child's classification, 51 p. cent in Group B and 8 p. cent in Group C. The routine operation was side-to-side portacaval anastomosis (75 p. cent). The operative mortality was 5.2 p. cent in all with 1 p. cent in cases with risk A, and 15 p. cent in cases with risk C. The fall in portal pressure was on average 15 cm of water, i.e. 41 p. cent of the initial pressure. The overall survival after 5 years was 65 p. cent, 70 p. cent for risk A and 26 p. cent for risk C. In 69 p. cent of cases the cause of death was liver failure. Encephalopathy, studied in 76 patients over an average period of 3 years, occurred in 39 p. cent of cases, and in 13 p. cent of the latter it was serious. In the 12 p. cent of survivors, we noted recurrent hemorrhage, but in only 2.5 p cent of cases did the bleeding definitely come from oesophageal varices. In the light of these results, the authors judge positively the surgical treatment of portal hypertension.
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PMID:[Immediate and late results of 171 therapeutic portal systemic by pass operations (author's transl)]. 30 46

The main clinical and laboratory findings in a group of 50 children with acute nephritis are described and discussed. All the group had evidence of a streptococcal aetiology. The wide spectrum of presenting complaints, the age distribution and the high incidence among Maori children are noted. The severity of the disease, as indicated by features such as hypertensive crisis, was greater than expected. Fifty per cent of our patients experienced one or more of our defined complications. Encephalopathy was seen in 12% of all patients and severe hypertension in 34%. The striking feature of the laboratory findings was the wide variation in complement changes. No constant patterns emerged which would have implicated either the "classical" or "alternate" pathway for the activation of complement in these patients. An unexpected finding was the relatively high incidence of a transient C3 nephritic factor in post-streptococcal cases. We found also that fibrin degradation products were present in high concentrations in the urine of patients with post-streptococcal nephritis, again an unexpected finding.
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PMID:Acute nephritis in fifty children: clinical and immunological studies. 33 59

Arterial hypertension, either transient or persistent, may be induced or aggravated by ingestion of various chemical agents, such as drugs, poisons, and food. Most of these agents either cause sodium retention and expand extracellular fluid volume or act as direct or indirect sympathomimetics. Others act directly on arteriolar smooth muscle. For a few agents, no precise mechanism has been ascertained. Hypertensive reactions may also occur as a result of drug interactions or food and drug interactions. In addition, paradoxical increases in pressure may be encountered during or after discontinuance of antihypertensive therapy. In general, these pressure increases are small and transient; however, a few have been associated with severe hypertension involving encephalopathy, strokes, and irreversible renal failure. Careful review of a patient's drug regimen, including over-the-counter preparations, may avoid chemically induced hypertension. Identification of any offending or incriminating agent will prevent the labeling of a chronic illness and obviate the need for lifelong antihypertensive therapy.
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PMID:High blood pressure. A side effect of drugs, poisons, and food. 37 59

The treatment of high blood pressure prevents death from congestive heart failure, hypertensive nephropathy, and encephalopathy, and strokes from cerebral arteriolar disease (lacunes, hemorrhage from microaneurysms). However, atherosclerosis, manifested as coronary artery disease is just as frequent a cause of death in well-controlled hypertensives as in poorly-controlled patients. Increasing evidence suggests that increased blood velocity, by causing turbulence and high shear rates at the endothelial surface of arteries, may be important in the pathogenesis of atherosclerosis. Turbulence has been observed in cerebral berry aneurysms. In order to measure the effects of antihypertensive agents on blood velocity, a new method of analysing Doppler ultrasound velocity recordings has been developed. Studies in Rhesus monkeys show the following: In doses which reduce diastolic pressure by 13-28%, propranolol decreased mean blood velocity (MV) by 17%, clonidine decreased MV by 14%, while methyldopa increased MV 12%, and hydralazine increased MV by 52%. (p less than .00001). It is hypothesized that enlargement of berry aneurysms, the progression of cerebral atherosclerosis, and embolism from carotid lesions might all be decreased by the selection of antihypertensive agents which decrease blood velocity.
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PMID:Effects of antihypertensive drugs on blood velocity: implications for prevention of cerebral vascular disease. 40 9

Serial EEGs with early and progressive bilateral periodic activity were recorded from a patient with clinically "atypical" but pathologically confirmed subcoritcal arteriosclerotic encephalopathy (Binswanger's type). This disease should be considered as a diagnostic possibility when periodic EEG activity is encountered, particularly when dementia, hypertension, and focal neurologic signs coexist. At times, white matter lesions may contribute to the production of periodic EEG activity.
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PMID:Periodic EEG activity in subcortical arteriosclerotic encephalopathy (Binswanger's type). 50 60

1 Six previously untreated emergency admissions to hospital with severe hypertension were given oral treatment with labetalol. 2 Pre-treatment diastolic BP exceeded 130 mmHg, and clinical evidence of either accelerated hypertension or encephalopathy was present. 3 Hypotensive response after treatment followed two patterns. 4 Quick-responders (n = 3) showed a sharp fall in BP to normal levels within 2 h, which was subsequently sustained for 10 or more hours. The daily dose of labetalol eventually required to achieve good BP control in this group was relatively low: 600--1200 mg. 5 Slow-responders (n = 3) showed a gradual, less marked fall in BP, which was sustained for many hours. These patients required further doses of labetalol to reduce BP to normal. The eventual daily dose of labetalol that ensured good BP control was high: 1200--2400 mg. 6 Heart rate was little changed by treatment. 7 Complications or side-effects were not observed.
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PMID:Acute management of severe hypertension with oral labetalol. 52

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.
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PMID:Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease). 56 79

The subcortical arteriosclerotic encephalopathy of Binswanger is characterized clinically by hypertension, dementia, spasticity, syncope, and seizures. It is usually diagnosed pathologically by the finding in white matter of diffuse demyelination or foci of necrosis plus arteriosclerotic and hypertensive vasculopathy. We present a case in which the diagnosis was made on the basis of the clinical course and a computerized tomogram which demonstrated extensive white matter degeneration. Postmortem examination confirmed both the diagnosis and the extent of the degeneration as shown by CT scan.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger): computerized tomography. 57 97


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