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

162 children with infantile spasms were treated with ACTH at the Children's Hospital, Helsinki, and at the Aurora Hospital, Helsinki, during 1960--76. In a large proportion (37%) of the children the treatment caused pronounced side effects, and the mortality was 4.9%. The most common complications were infections: septic infections, pneumonias, and urinary and gastrointestinal infections. Other side effects were arterial hypertension (11), osteoporosis (2), hypokalaemic alkalosis (2), and other marked electrolyte disturbances (10). In children necropsy showed fresh intracerebral haemorrhages. Four children developed oliguria and hyperkalaemia during and after withdrawal of ACTH. One of them had tubular necrosis confirmed by renal biopsy. Infections were significantly more common with large doses (120 units) of ACTH than with small ones (40 units). It is concluded that side effects, even severe ones, are more common during treatment than had been assumed. Careful watch is important before and after treatment. The benefit of very high dosages should also be reconsidered.
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PMID:ACTH therapy in infantile spasms: side effects. 625 50

In order to determine the relative roles of O2 tension and content, CO2 tension, hydrogen ion concentration, arterial blood pressure, and cardiac output in the regulation of fetal cerebral blood flow (CBF), we used radioactively labeled microspheres to measure flow to 20 major brain regions in 24 chronically catheterized fetal lambs. We continually monitored fetal heart rate and blood pressure, and periodically measured arterial PO2, PCO2, pH, and hematocrit. In addition to CBF measurements during control periods, we measured CBF during: 1) hypoxia (O2 content less than 6 ml X dl-1; O2 tension less than 15 torr) induced by having the ewe breathe a gas mixture with low O2 concentration, 2) hypercapnia (PCO2 greater than 50 torr) induced by increasing the maternal inspired CO2, 3) acidosis and alkalosis (7.60 greater than pH greater than 6.60) induced by infusing lactic acid or bicarbonate into the fetus, and 4) hypotension (blood pressure less than 35 mm Hg) and hypertension (blood pressure greater than 55 mm Hg) induced by rapidly phlebotomizing or transfusing the fetus. We used multiple regression analysis and analysis of covariance to examine the dependence of total cerebral blood flow on arterial O2 tension and content, CO2 tension, pH, blood pressure, and cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow: studies in the fetal lamb during hypoxia, hypercapnia, acidosis, and hypotension. 644 Nov 42

In normotensive Wistar rats of a random-bred strain and in spontaneously hypertensive rats (SHR) of the Okamoto-Aoki-strain, the mean systemic arterial blood pressure, the pO2, pCO2, pH-values and the base excess of the arterial blood were measured during ventilating normal air as well as hypoxic (12.6% O2 in N2) and hyperoxic (100% O2) gas mixtures. The animals were anaesthetized and breathed spontaneously; they aged 5-6, 15-20, 30-40, and 50-70 weeks. The volume of their carotid bodies was determined morphometrically. When compared with the age-matched normotensive controls at an age of 5-6 weeks the SHR already exhibited slightly but significantly elevated blood pressures but had equal carotid body size and arterial carbon dioxide tension. In contrast, hypertensive animals in the established phase of hypertension (older than 15 weeks) showed greater carotid bodies and a highly significant respiratory alkalosis when compared with the corresponding age-group of the normotensive rats. The reactions of the mean systemic arterial blood pressure and the arterial pCO2 provoked by hypoxia and hyperoxia proved to be age-dependent in both the normotensive and hypertensive animals but this influence of age was different in the two strains of rats. The data support the concept that alterations of arterial chemoreceptor structures and reflex effects found in the established phase of hypertension are the result of this disease. Furthermore they indicate that, when interpreting arterial chemoreceptor reflex effects in hypertensive humans and animals, the stage of hypertension must be taken into account.
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PMID:Influence of age on carotid body size and arterial chemoreceptor reflex effects in spontaneously hypertensive (SHR) and normotensive rats. 673 56

The parameters of the acid-base-state of the arterial blood were measured in spontaneously hypertensive rats of the Okamoto-strain (SHR) and in normotensive Wistar rats (NWR) of a random-bred strain. The animals were anaesthetized with chloralose-urethane and breathed normal air under sea-level conditions. Structure and size of their carotid bodies were studied by light-microscopic methods. When compared with the NWR, the SHR showed a respiratory alkalosis and enlarged carotid bodies. In the SHR, never in the NWR, the lumen of the branches of the glomic arteries was narrowed by pad-like structures. The data suggest that systemic hypertension leads to morphologically and functionally detectable alterations of both carotid body structure and function. The interdependence of arterial chemoreceptor activity, sodium household, and the adjustment of systemic arterial blood pressure is briefly discussed.
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PMID:The carotid bodies of spontaneously hypertensive rats (SHR): a functional and morphologic study. 680 Jan 71

Reference is made to the picture observed in two patients with flaccid tetraparesis, severe hypopotassaemia, and myoglobinuric muscle necrosis (hypokalaemic myopathy). Recent onset of hypertension was a feature of both cases. Initially, however, no reason could be assigned for this, nor for the massive loss of potassium. Numerous investigations in the first case (and relatively quick verification in the second) incriminated a steroid, 9-alpha-fluoroprednisolone acetate, in a nasal spray. This has often been reported as the cause of an iatrogenic syndrome due to excess of mineral corticoids, with hypertension, hypokalaemia and alkalosis, suppression of plasma renin activity, and reduction of blood and urinary aldosterone, all of which were observed in these two patients. Withdrawal of the drug and treatment with potassium chloride led to relatively rapid normalisation of the serum electrolytes. Recovery of muscle strength took place after about 20 days, almost at the same time as the normalisation of muscle enzymes. Hypertension, on the other hand, regressed slowly. The nexus between chronic use of the spray and the occurrence of hypokalaemic muscle necrosis is examined in detail. Stress is laid on the importance of specific investigation of the prior use of intranasal steroids in the differentiation of muscle disturbances due to potassium depletion.
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PMID:[Hypokalemic myopathy caused by fluoroprednisolone in a nasal spray. Observations 2 cases]. 685 55

This paper reviews and presents data from a series of studies evaluating the extent of potassium depletion that occurs in various disease states and a comparison of the efficacy of potassium supplementation or potassium sparing diuretics in its correction. Changes in serum potassium levels are common after diuretics but are relatively minor in most people if small doses of diuretics are used. Total body potassium deficit is uncommon in people treated with a diuretic for hypertension and the fall in serum potassium results from alkalosis and a shift of potassium into the cell. Potassium sparing diuretics correct the potassium abnormality more readily than potassium supplements. Evidence is also presented that suggests that a high salt, low potassium diet may be an important cause of hypokalemia in people given diuretics.
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PMID:Potassium maintenance. Potassium supplements or potassium sparing agents. 694 35

A 4-yr-old boy with hypertension and hypokalaemic alkalosis had low plasma aldosterone levels and renin activity. The hypertension and hypokalemia responded to spironolactone and triamterene therapy. A partial response to dexamethasone was observed. Analysis of urinary steroid metabolites by gas chromatography-mass spectrometry showed that the excretion of metabolites of deoxycorticosterone and aldosterone was subnormal, and there was no evidence for sizeable excretion of unusual steroids with potential mineralocorticoid activity. The cortisol excretion rate, however, was subnormal, and the relative excretions of individual metabolites of this hormone were not typical. In particular, the excretion of tetrahydrocortisone was markedly reduced, and the excretions of allotetrahydrocortisol and free cortisol and metabolites were elevated. These findings suggest that modified or deficient metabolism of adrenal steroids could give rise to elevated blood pressure. It is not known whether the inappropriate production of unusual cortisol metabolites were responsbile for the high blood pressure or whether the altered metabolism is indicative of similar abnormality in the metabolism of other adrenal steroids, resulting in hyperproduction or extended half-life of minor but highly active mineralocorticoids of unknown structures.
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PMID:Hypertension in a four-year-old child: gas chromatographic and mass spectrometric evidence for deficient hepatic metabolism of steroids. 698 56

Criteria for the screening, diagnosis and therapy of primary aldosteronism (PA) were defined on the basis of its symptoms analysis in 40 PA patients. A diagnosis of PA was proved in 4.12% of 970 patients admitted for arterial hypertension. The presence of polyuria, nocturia, neuromuscular disorders, hypertension, hypopotassaemia, alkalosis, elevated urinary potassium excretion, improving after Spironolactone, was most valuable for the purposes of screening. High plasma aldosterone concentration (PAC) and suppressed renin activity (PRA) provided evidence of the presence of PA. The most successful technique to differentiate aldosterone producing adenoma (APA) from idiopathic hyperaldosteronism (IHA) proved to be adrenal phlebography combined with determination of PAC in the adrenal veins. APA was associated with a 5.9 fold higher PAC in the vein of the adenoma - affected adrenal in contrast with a symmetric PAC rise in both adrenal veins in IHA. A paradoxical decrease of PAC occurred in the peripheral blood of most patients with APA after standing up, but 23.8% exhibited the same orthostatic increase as IHA patients. In all APA patients, unilateral adrenalectomy eliminated the symptoms of hyperaldosteronism and improved or cured hypertension. Spironolactone was indicated preoperatively for all surgical candidates, for non-operated APA patients, and for all IHA patients.
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PMID:Primary aldosteronism -- screening, diagnosis and therapy. 702 94

A 19-month-old boy presented with failure to thrive and polydipsia. Low-renin hypertension was diagnosed by the presence of hypertension, hypokalaemic alkalosis, suppressed plasma renin activity and low plasma aldosterone. Plasma levels and urinary excretion of other mineralocorticoids and glucocorticosteroids were low or normal. Urinary tetrahydrocortisol (THF) was increased relative to tetrahydrocortisone (THE) and also the plasma cortisol to cortisone ratio was elevated. These findings are suggestive of a decreased activity of cortisol-11 beta-hydroxysteroid dehydrogenase. Hypertension and hypokalaemia were not influenced by spironolactone and dexamethasone. Triamterene normalised serum potassium, but addition of furosemide was required for lowering blood pressure. With this treatment catch-up growth was observed.
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PMID:Low-renin, low-aldosterone hypertension and abnormal cortisol metabolism in a 19-month-old child. 704 81

Primary aldosteronism, when caused by an aldosterone-producing adenoma, is a surgically treatable condition. An operation was performed on a 44-year-old patient with this condition. The pre-operative preparation and anaesthetic management are presented. The specific problems of hypertension, hypokalaemia, hypokalaemic alkalosis and renal lesions, and their importance to the anaesthetist are discussed.
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PMID:An aldosterone-producing adrenal cortical adenoma. 712 66


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