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

Subarachnoid hemorrhage induces a lot of extracerebral disturbances such as: systemic hypertension, electrocardiographic abnormalities both morphological, rhythmic and subendocardial damages; those events have been interpreted as overactivity of the sympathetic nervous system. In biochemical changes, hyponatremia early recognized was referred during a long time to a syndrome of inappropriate secretion of antidiuretic hormone. Hyponatremia is now referred to a cerebral salt-wasting. Hypovolemia often observed supports the use of volemic expansion in the prevention and treatment of ischemic complications associated with ruptured intracranial aneurysms. The hypothalamus which lies in close anatomical proximity to the circle of Willis may be directly influenced by the rupture of a cerebral aneurysm. So, hypothalamic dysfunction may affect pituitary adrenal function sympathetic and parasympathetic activities. The knowledge of all these disturbances, and their mechanisms supports the current strategies for the management of aneurysmal subarachnoid hemorrhage.
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PMID:[Physiopathology of meningeal hemorrhage caused by aneurysmal rupture: extracerebral aspects]. 228 35

beta-Blockers reduce hypertension effectively and safely. However, their overall efficacy is a balance between their influence on blood pressure and their influence on other important risk factors. Thus, whereas a drug may ameliorate the primary blood pressure marker of the syndrome, this effect may be negated by enhancement of aggressive cofactors. The evolution of the beta-blockers exemplifies how this potentially dangerous conflict may be counteracted. The latest "third-generation" agents, such as celiprolol, not only achieve their primary objective of lowering blood pressure, but also have the potential to simultaneously reverse some of the deleterious cofactors. For example, celiprolol reduces the threat of atheroma by lowering serum cholesterol, and enhances the efficacy of myocardial oxygen utilization in heart failure by reducing plasma triglyceride metabolism. Its ability to reduce fibrinogen and its lack of effect on glucose metabolism are additional positive factors. Celiprolol also provides the combined pharmacodynamic advantages of vasodilatation and inotropic support of the heart, and it attenuates the myocardial oxygen-wasting effects of sympathoadrenal stimulation. These attributes all make a positive contribution to cardiovascular risk reversal in the hypertensive patient.
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PMID:Celiprolol and risk factor reversal in hypertension. 248 88

When a patient with chronic obstructive pulmonary disease (COPD) requires medical therapy for systemic hypertension, a number of special considerations may affect the choice of antihypertensive drug and subsequent management. Thiazide diuretics have no adverse effect on airway function and are the agents of choice for initial therapy. beta-Antagonists are usually considered first-line agents in antihypertensive therapy, but even relatively cardioselective ones may increase airway resistance in patients with obstructive lung diseases, and they should be used with caution, if at all, in such patients. Although potassium-wasting diuretics are the preferred agents for treating hypertension in patients with COPD, they may worsen carbon dioxide retention in hypoventilating patients and potentiate hypokalemia in those receiving corticosteroids. In addition, beta-agonists may substantially lower serum potassium levels in patients already rendered hypokalemic by diuretics. Patients with COPD receiving potassium-wasting diuretics who have chronic respiratory acidosis or are receiving corticosteroids or beta-agonists should undergo close monitoring of electrolyte levels and be considered for therapy with potassium supplements or, preferably, potassium-sparing agents.
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PMID:Fluid and electrolyte considerations in diuretic therapy for hypertensive patients with chronic obstructive pulmonary disease. 286 47

Numerous studies have shown that longterm oxygen therapy in hypoxaemic patients with chronic airflow obstruction (BPCO) is capable of improving the prognosis and decreasing the risk of cardio-respiratory decompensation; in addition sometimes physical capacity and intellectual capacity is improved. Another result often noted is a reduction in the mean hospital stay which corresponds to an improvement in the quality of life. A PaO2 constantly below 55 mmHg (7.3 kPa) is defined by the majority of authors as a precarious state. At this level even a small change in alveolar ventilation or disturbance of distribution would lead to an important fall in the oxygen content of the arterial blood. The stability of the PaO2 during the weeks of respiratory reeducation with specially controlled medical treatment, as well as the willing consent of the patient and his family, are indispensable conditions for the prescription of OLT. When hypoxaemia is of moderate severity (PaO2 between 50 and 60 mmHg (6.6-8 kPa), prolonged medical treatment (with abstention from tobacco) for at least two months is advised and a study of complementary criteria to further validate the indications for oxygen. Such features would include a worsening of the hypoxaemia during exercise of 30 to 40 watts (PaO2 less than 50 mmHg, 6.6 kPa), an elevated haematocrit (greater than 55%), a rise of the P (A-a)O2 (greater than 30 mmHg or 4 kPa), a nocturnal desaturation even in the absence of apnoea (oxyhaemoglobin saturation (SaO2) of less than 80% for more than 50% of the time asleep). Added to these criteria are the radiological, echographic and clinical signs of the effect of hypoxaemia on the pulmonary circulation. Frank pulmonary arterial hypertension observed in hypoxaemia of moderate severity when the PaO2 is in the region of 55 mmHg and is an argument for the prescription of OLT. Amongst the developing criteria, exacerbations of respiratory encephalopathy, intellectual deterioration, progressive wasting, permanent ventilatory embarrassment with tachypnoea, should be borne in mind as the occasion arises. A schedule of 18 hours per day (without stopping for more than 3 hours) is necessary to obtain an improved survival and places a great demand on patient co-operation and on their environment. A prolonged educational programme is required. To achieve such a schedule the use of portable oxygen may be justified so that patients can lead a normal social life.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Critical study of the indications for long-term oxygen therapy. Chronic obstructive bronchopneumopathies]. 314 Mar 16

To determine the significance of hypertension in the pathogenesis of berry aneurysms, 113 patients with subarachnoid haemorrhage (SAH) and verified aneurysm and 63 patients with SAH without aneurysm were compared. Of those patients with angiographically verified aneurysms, 61.9% were found to have elevated blood pressure (greater than 160/95 mmHg) and 19.5% showed electrocardiographic signs of left ventricular hypertrophy (SV1 + RV5 (6) greater than 3.5 mV). The percentages for patients without aneurysm were 36.5% and 6.4% respectively. A significant correlation was found between anterior aneurysms and left ventricular hypertrophy (P less than 0.01). The mean Sokolow index values were also significantly elevated in cases of aneurysm (P less than 0.01). There was a complementary relationship between the extent of left ventricular hypertrophy and the percentage of females with regard to localization of an aneurysm and age group. The predominance of females in the total aneurysm population, in the 50- to 59-year-old age group, and among patients with internal carotid aneurysms indicates that a sex-specific hormonal factor may also play a role in the pathogenesis of aneurysms in addition to hypertension. The collagen wasting commonly observed in bone and skin in the post-menopausal period due to decreased oestrogen levels could possibly be responsible for the formation of aneurysms in the proximal segments of the cerebral arteries, as occurs in various connective tissue diseases.
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PMID:Direct evidence of hypertension and the possible role of post-menopause oestrogen deficiency in the pathogenesis of berry aneurysms. 316 Aug 33

The incidence of acute renal failure, hypertension and electrolyte disorders in 64 bone marrow transplant recipients randomized to receive either cyclosporin or cyclophosphamide was investigated. Sixty-four per cent of patients developed acute renal failure, 75 per cent hypertension, and 88 per cent significant hypomagnesemia. The incidence of diastolic hypertension and hypomagnesemia was greater in the patents treated with cyclosporin. Hypomagnesemia was due to magnesium wasting by the kidney. Both groups received similar cumulative doses of aminoglycoside antibiotics. Significant proteinuria developed in all but one patient and nephrotic-range proteinuria was noted in 21 per cent. The cause of the proteinuria is unclear; no obvious morphologic changes were seen at autopsy in patients who exhibited nephrotic-range proteinuria. The abnormalities of renal function were shown to be transient in patients who were observed for periods ranging from one to three years. It is concluded that hypertension, renal failure and hypomagnesemia are common in the setting of bone marrow transplantation. Whereas cyclosporin probably aggravates the severity of these disorders, it is likely that other factors (e.g., aminoglycoside antibiotics) play a major role as shown by the high incidence of renal and electrolyte disorders in patients treated with cyclophosphamide alone.
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PMID:Hypertension and renal dysfunction in bone marrow transplant recipients. 327 85

Cyclosporine is known to cause hypertension, and we have recently reported that it causes hypomagnesemia and renal magnesium wasting in marrow transplant recipients. We performed a case-control study to ask whether hypomagnesemia might be related to this form of drug-induced hypertension. The charts of 188 patients treated with cyclosporine were evaluated for the development of hypertension. The 32 patients who became hypertensive were age, sex, and disease-matched with 32 cyclosporine-treated controls. Baseline serum Mg levels were normal in both groups. However at the time of development of hypertension, the hypertensive patients had a mean (+/- SD) Mg of 1.22 +/- 0.20 mEq/L versus controls 1.40 +/- 0.33 mEq/L (P less than 0.01). Serum calcium, albumin, creatinine, potassium, and cyclosporine concentrations were not different between the two groups. This study may indicate that hypertension and hypomagnesemia are coincident toxicities in cyclosporine-treated patients. Alternatively, our data support the hypothesis that acquired derangements in magnesium metabolism may contribute to the development of hypertension. Magnesium replacement may prove beneficial in the treatment and/or prevention of cyclosporine-associated hypertension.
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PMID:Correlation of hypomagnesemia with the onset of cyclosporine-associated hypertension in marrow transplant patients. 351 Apr 94

A family is described in which autosomal recessive inheritance of retinitis pigmentosa and chronic renal failure occurred. Several features, including late onset of renal failure, lack of salt wasting, the presence of hypertension and blindness in the sixth decade, are unusual and suggest that this may be a previously undescribed syndrome.
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PMID:A family with retinitis pigmentosa and ESRD with late presentation, hypertension and absence of polyuria or salt wasting. 369 52

By defining a model for control of potassium homoeostasis, patients with unexplained hypokalaemia may then be described as fitting or not fitting the model. Fitting the model implies an abnormality of known control mechanisms (e.g. aldosterone); by contrast, not fitting the model suggests other unknown factors responsible for the hypokalaemia and, possibly, hypertension. In the presence of normal acid-base status, potassium excretion (UK+V) is regulated by plasma potassium (PK+), delivery of sodium to the distal tubule and aldosterone secretion. A linear relationship (correlation coefficient of 0.72) was defined by: UK + V/PK+ = 5.1 X log(UAldoV) X log(UNa+ V) + 1.4 based on a 24 h urine collection and plasma sample, in 16 normal subjects, 50 hypertensive normokalaemic subjects and 11 patients with hyperaldosteronism. The relationship was robust and held true for variations in dietary sodium and potassium intake (5-300 and 20-100 mmol/day respectively) and variations in aldosterone excretion produced by enalapril. Patients with abnormal renal potassium wasting due to known extraneous factors (n = 11) all fell outside the 95% confidence limits. Twelve patients with hypertension and hypokalaemia and renal potassium wasting all fitted within the confidence limits, being no different from 22 controls selected on the basis of age and urinary potassium excretion (30-50 mmol/day). This suggests that in these 12 patients the hypokalaemia (but not necessarily the hypertension) was not due to 'unknown' steroids but rather lack of regulation of the controlling variable, aldosterone.
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PMID:A simple method for definition of incomplete suppression of aldosterone and its association with hypertension and hypokalaemia in man. 375 36

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
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PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15


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