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

The syndrome of autonomic dysreflexia often occurs in quadriplegic subjects and is characterized by paroxysmal hypertension, headache, vasoconstriction below and flushing of the skin above the level of transection, and bradycardia. These attacks may cause hypertnesive encephalopathy, cerebral vascular accidents, and death. In five patients during crises, the mean arterial pressure changed from 95 to 154 mm Hg, heart rate 72 to 45 beats/min, cardiac output 4.76 to 4.70 L/min, and peripheral resistance 1650 to 2660 dynes.sec.cm-5. In eight subjects the control plasma, red cell, and total blood volumes were 19.1, 10.5, and 29.6 ml/cm body height, respectively, and when hypertensive, the plasma protein concentration increased by 9.9% and the hematocrit by 9.5%. Plasma volume was only reduced by an estimated 10-15%. At that time, arterial dopamine-beta-hydroxylase (DbetaH) activity increased 65% and prostaglandin E2 concentration by 68%. Thus, the augmented DbetaH activity presented primarily an elevated sympathetic tone and not hemoconcentration of that protein. The rise in prostaglandin may contribute to the severe headaches during hypertensive episodes.
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PMID:Hypertensive crises in quadriplegic patients. Changes in cardiac output, blood volume, serum dopamine-beta-hydroxylase activity, and arterial prostaglandin PGE2. 61 23

Nineteen patients with severe essential hypertension or hypertension due to renal parenchymal disease were treated with intravenous clonidine. In 14 patients the elevated blood pressure was complicated by one or more crises: left ventricular failure in seven patients, encephalopathy in six, and subarachnoid hemorrhage, cerebral hemorrhage, dissecting aortic aneurysm, acute renal failure, and severe epistaxis, one episode each. Clonidine 0.15 or 0.30 mg, was given intravenously every 40 minutes until the diastolic blood pressure was decreased to 120 mm Hg or below. Blood pressure was taken every 10 minutes. Both systolic and diastolic blood pressure were reduced significantly after intravenous clonidine, the former by 96 mm Hg (P less than 0.001), the latter by 52 mm Hg (P less than 0.001) within a period of 40 minutes to 2 1/2 hours. The clonidine dose varied from 0.15 to 0.90 mg, mean 0.52 mg. Heart rate was decreased significantly by 20 beats/minute (P less than 0.001) by the drug. Serious side effects were not observed except for an episode of transient sinoatrial block. Renal function was not affected. Patients who were on chronic diuretic therapy prior to treatment with intravenous clonidine showed a significantly greater decrease in both systolic (P less than 0.01) and diastolic (P less than 0.001) blood pressure after the first clonidine dose. In one patient intravenous clonidine was not effective (i.e., blood pressure remained 200/150 mm Hg) in spite of a total clonidine dose of 0.9 mg. Two patients died, one from severe cerebral hemorrhage, the other from an extensive dissecting aortic aneurysm, but the fatal outcome was not related to clonidine.
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PMID:Evaluation of intravenous clonidine in hypertensive emergencies. 63 67

The hypertensive encephalopathy is a syndrome consisting of a sudden elevation of arterial pressure usually preceded by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. The syndrome may complicate acute glomerulonephritis, toxemia of pregnancy and essential or malignant hypertension. Two syndromes must be differentiated from true hypertensive encephalopathy: 1. acute anxiety state with labile hypertension and 2. acute pulmonary edema due to hypertensive heart disease. At least in patients with acute anxiety states, the use of antihypertensive agents is usually not indicated. Since encephalopathy is always accompanied by increased vascular resistance and since clinical experience has demonstrated clearing of the sensorium, cessation of convulsions and release of vasoconstriction following reduction of blood pressure, the primary aim of therapy should be prompt lowering of arterial pressure. The two agents of choice are diazoxide and sodium nitroprusside. Stroke is differentiated from encephalopathy by the persistence of lateralizing signs. The aggressiveness of antihypertensive therapy in this situation depends on the severity of the hypertensive process. Rapid reduction of blood pressure is indicated in patients found to have accelerated hypertension while a more gradual lowering of pressure appears warranted for patients with chronic arterial hypertension and evidence of generalized arteriosclerosis.
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PMID:Management of hypertensive encephalopathy. 72 Oct 56

Frequently the first clinical sign of neuroblastoma is not caused by local or metastatic tumor growth but is a paraneoplastic symptom (PNS). Such PNS are fever, diarrhea, hypertension, weakness of muscles, Horner's syndrome and myoclonic encephalopathy. Certain PNS disappear with tumor removal, other do not. The clinical importance of PNS is the prognostic and especially diagnostic value. The pathogenetic relations between tumor and PNS as discussed in the literature are interesting but mostly speculative. Effects of Catecholamines and/or immunologic reactions are thought to be the most probable cause of PNS.--The article is based on current literature; in addition, two short case histories are presented.
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PMID:[Paraneoplastic symptoms of neuroblastoma (author's transl)]. 77 98

Remission followed prednisolone therapy in 9 out of 21 Nigerian children with the nephrotic syndrome who had highly selective proteinuria (CG/CA less than 15%). Of these, 5 patients have remained well off all treatment during a follow-up of nearly 5 years, 4 have relapsed more than once but have responded to further courses of prednisolone. 3 of 21 with less selective proteinuria also remitted but all relapsed and only one of these has responded again. The other two have relapsed and further courses of prednisolone have not totally abolished their proteinuria though they are asymptomatic and in good health. Toxicity (hypertension, sometimes with encephalopathy and infection) was commoner in the patients with less selective proteinuria treated with steroids than in those with highly selective proteinuria. 3 steroid-sensitive patients who had had repeated relapses became free from relapse off all treatment after a course of cyclophosphamide, given during steroid-maintained remission. All but 2 of the renal biopsies taken were regarded as abnormal. The lesions were less severe in those who responded than in those who did not. There is some evidence to suggest that Plasmodium malariae may be a cause of some of the steroid-sensitive disease, as well as the steroid-resistant.
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PMID:Differential protein clearances and response to treatment in Nigerian nephrotic children. 79 39

Irreversible brain damage after a short period of cerebral ischemia is a clinical drama. Not neuronal dead in se, but a hemodynamic event, described as no reflow phenomenon (NRF) seems to be the primary pathogenetic factor towards fatal outcome. A combination of four flow promoting therapeutic measures (heparinisation, hemodilution, systemic arterial hypertension and brainflushing with dextran 40) greatly improves recovery of the brain function after 12 min. of cardiac arrest in dogs. Short acting barbiturates provide remarkable amelioration of postischemic encephalopathy in the monkey.
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PMID:Recent advances in the treatment of postischemic encephalopathy. A review. 82 14

We have documented a highly significant increment in hepatic arterial flow following a portacaval shunt in patients with cirrhosis of the liver and portal hypertension. In contrast with other hemodynamic variables, the increment in arterial flow was directly related to morbidity, hospital mortality, and long term survival. Patients with increments smaller than 100 ml/min had the worst clinical results. They accounted for all of the hospital mortality, the largest incidence of encephalopathy, and the worst long term cumulative survival rates. The extent of the increment was not related directly to the type of shunt but, rather, to some intrinsic capability of the cirrhotic liver to increase its arterial flow in response to the relief of sinusoidal hypertension produced by the shunt. This capablilty appears related to the degree of entrapment of the hepatic arterioles by the fibrous tissues of cirrhosis. This encasement of arterioles should change the elastic properties of the hepatic arterial bed and we propose to measure these properties by determining the characteristic input impedance of the arterial bed.
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PMID:Hepatic artery flow improvement after portacaval shunt: a single hemodynamic clinical correlate. 96 97

A 51-yearold man with moderate intermittent hypertension had a rapidly progressive, profound dementia in the absence of significant localizing neurological signs. Postmortem examination disclosed the vascular alterations and diffuse white matter degeneration which characterize subcortical arteriosclerotic encephalopathy (SAE) or Binswanger's disease. The case underscores the need to consider vascular disease as an etiology of dementia -- even in the absence of focal neurological deficit.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's disease). A vascular etiology of dementia. 100 40

Effects of chlorhydrate of Ketamine upon CSF pressure were studied in 10 patients with different intracranial pathology. In opposition to the results of other authors, in 5 patients there was no increase of pressure after the drug was applied. This difference is ascribed to the individual pathology of the patients studied, emphasizing that 4 of them were bearers of a diffuse vascular encephalopathy with intelectual damage, added to an acute vascular accident in 3 cases. For these reasons, it is presumed that a deficient auto-regulation of cerebral circulation, with diminished vasomotor reactivity, is reasponsible for the absence of hypertension after application of the drug. The study of the variations of cerebrospinal fluid pressure after chlorhydrate of Ketamine is applied may enable to measure the efficiency of the mechanisms of auto-regulation in any determined patient.
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PMID:[Effects of ketamine on the pressure of the cerebrospinal fluid. Variations of its effects]. 105 95

Histiocytosis X describes a disease characterized by histiocytic infiltration of the reticuloendothelial system, skin, bones, and pituitary gland. The disseminated form frequently occurs in infants and children. Chemotherapy has significantly improved the prognosis in this disorder. Sixty-three per cent of survivors, however, have some residual disability related to fibrosis of tissues previously infiltrated by histiocytes. In instances of liver involvement, healing by fibrosis may result in cirrhosis with portal hypertension and bleeding esophageal varices. Clinical findings include hepatosplenomegaly, jaundice, ascites, hypoalbuminemia, prolonged prothrombin time, and Bromsulphalein retention. Histologic examination of the liver shows a characteristic dense "macronodular" periportal cirrhotic pattern. Three children with portal hypertension and bleeding varices due to healed histiocytosis X were sucessfully managed by portosystemic shunt procedures. Portacaval, mesocaval, and central splenorenal shunts were equally effective in relieving poral hypertension. These children had neither recurrence of bleeding nor evidence of encephalopathy. Two children remain well whereas in one patient a primary hepatoma developed fourteen years posthung and he died of pulmonary metastases. Portosystemic shunt procedures effectively relieve the threat of potentially fatal variceal hemorrhage and improve the opportunity for long-term survival in children with cirrhosis and portal hypertension due to healed histiocytosis X.
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PMID:Portal hypertension in infants and children with histiocytosis X. 108 50


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