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

Continuous measurements of intracranial, pressure were conducted by the extradural method in 40 patients with various types of skull trauma. A correlation was demonstrated between the value of this pressure and the clinical condition of the patient only with high values of the pressure, in which nearly always wave-like pressure changes were observed. The occurrence of wave-like changes was a more reliable sign of threatening cranial hypertension than the value of intracranial pressure. Continuous measurement of pressure during intravenous administration of glycerol demonstrated that a significant fall of pressure preceded the regression of clinical signs of intracranial hypertension.
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PMID:[Our evaluation of clinical usefulness of continuous extradural measurement of intracranial pressure in patients with cranio-cerebral injuries]. 663 2

A heat-balance study was carried out on conscious rabbits exposed to ambient temperatures (Ta) from 8 degrees to 40 degrees C. At Ta = 40 degrees C, heat gain exceeded heat loss and led to hyperthermia and heat stroke, and the latency for the onset of heat stroke was found to be around 87 minutes. At the onset of heat stroke, the comatose animals showed higher levels of rectal temperature, ear skin blood flow, respiratory evaporative heat loss, metabolic rate, intracranial pressure (ICP), and cerebral water content as compared to those of control animals (kept at an ambient temperature of 24 degrees C). Before the start of heat stress, the animals had an average mean arterial blood pressure (MABP) of 94 mm Hg and cerebral perfusion pressure (CPP) of 80 mm Hg. However, at the onset of heat stroke, the average MABP and CPP decreased to 67 and 19 mm Hg, respectively. The reduction in CPP at the onset of heat stroke was due to both a decrease in MABP and an increase in ICP. In addition, the comatose animals which received an intravenous infusion of 10% glycerol (3 ml/min) had a survival time (interval between onset of heat stroke and death) longer than that of the comatose animals which received the control-vehicle solution. The prolongation of survival time in the glycerol-treated animals may be due to lower rectal temperature, lower cerebral water content, or lower ICP during the development of heat stroke. The present data indicate that not only hyperthermia but also cerebral edema, intracranial hypertension, decreased MABP, and decreased CPP are the main causes of heat stroke. The therapeutic values of glycerol on heat stroke may be related to the depressant action on cerebral edema, intracranial hypertension, and body temperature.
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PMID:Experimental study on the pathogenesis of heat stroke. 672 68

Taking into consideration the frequent combination of hypertension, ischaemic heart disease and heart insufficiency the effect of blood pressure as well as the influence of pre- and afterload gain increasing importance, when nitrates are used. It is the question, whether the blood pressure reducing effect may be used with a certain aim or not. In own investigations acute haemodynamic experiments with glycerol trinitrate were carried out on 10 patients with arterial hypertension (catheterization, estimation of HMV and so on) in rest and under ergometric load, clinical therapeutic experiments on 10 patients with crisis of hypertension with cerebral and/or cardiac complications as well as long-term experiments with pentaerythrityl tetranitrate on 6 patients with in most cases severe arterial hypertension. The acute effects on the haemodynamics correspond to those in normal blood pressure, in which case the reduction of blood pressure and resistance is more expressed. The favourable effect of glycerol trinitrate in the crisis of hypertension with cardiovascular complications can be regarded as proved. First own experiences with the long-term application of nitrates do not yet result in a clear estimation of effectivity and indications.
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PMID:[Treatment of severe hypertension and hypertensive crises with nitrates]. 678 73

Acute intracranial hypertension may respond to intravenous mannitol, but frequent administration can cause cerebral edema or renal problems. We evaluated the use of 20% glycerol administered intravenously as an alternative to mannitol. Intravenous glycerol and mannitol were equally effective in lowering acute elevations of intracranial pressure. The duration of effect was similar for both agents. Side effects of intravenous glycerol were related to concentration, rate, and frequency of administration. In severe encephalopathies, such as Reye syndrome, we recommend infusions of 20% glycerol or 20% mannitol at a dose of 0.5-1.0 gm per kilogram. Glycerol should be administered in 0.45% or 0.9% saline, no faster than 1.5 ml (3.3 mOsm) per minute.
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PMID:Intravenous glycerol and mannitol therapy in children with intracranial hypertension. 680 42

Intracranial hypertension is caused by various pathologic processes. From oncologic point of view, they are 1) intracranial space-occupying lesions, especially malignant tumors, 2) leptomeningeal tumors, 3) hemorrhage in the brain tumors, 4) intracranial hemorrhage due to hemorrhagic diathesis related to the malignant tumors, and 5) cerebral thrombosis or embolism due to increased blood coagulability secondary to malignancy. In the increase of intracranial pressure, brain edema or disturbance of cerebrospinal fluid (CSF) circulation due to the presence of brain tumors play more important role than the tumor bulk itself. CT scan is useful for demonstrating the process causing the intracranial hypertension. Therapeutic measures in all patients with increased intracranial pressure are initiated promptly to restore the cardiopulmonary dysfunction if any. Hyperventilation and intravenous infusion of hyperosmolar agents such as mannitol and glycerol have an immediate effect in reducing intracranial pressure when brain edema plays role in increasing it. Steroids are also very effective in reducing brain edema; the effect is less immediate but long lasting. CSF drainage or shunt operation is necessary when dilated ventricular system plays role in the intracranial hypertension. The radical treatment of the intracranial hypertension is a removal of the tumor causing it; however, if not indicated, the second choice is the internal or external decompressions. Postoperative radiotherapy and chemotherapy are also indicated for the malignant brain tumors.
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PMID:[Intracranial hypertension]. 688 68

Labetalol was given to women with hypertension of pregnancy in their last trimester to study its acute effect on circulation and metabolism. Seven women were given 50 mg labetalol i v. There was a significant decrease of blood pressure from a mean of 143/101 +/- 4/2 (SEM) to 127/88 +/- 5/2 mm Hg. Maternal heart rate fell significantly from 77 +/- 5 to 68 +/- 3 beats per min. These changes persisted during a three-hour observation period. The hypotensive response was accompanied by a significant increase in plasma noradrenaline from 1.54 +/- 0.16 to 2.37 +/- 0.41 nmol/l, suggesting sympathetic activation. Plasma cyclic AMP, which is increased by beta 2-adrenoceptor stimulation, was significantly elevated after labetalol. This supports the hypothesis of partial beta-agonist activity of labetalol. Lipid metabolism, as judged from measurements of plasma FFA, glycerol and 3-hydroxybuturic acid, showed little change. The acute effect of labetalol on uteroplacental blood flow was determined in eight women with pregnancy hypertension using a gammacamera on line with a computer. 0.5 mCi indium-113m was given i v before and 30 min after labetalol was administered i v in a dose of 1 mg per kg body weight. After the injections of indium-113m, serial scintigrams were recorded during 10 s periods for 240 s. By computerized summation of the scintigrams, an image was obtained in which the placenta could be outlined for time-activity analysis of the isotope accumulation curve. From this curve a uteroplacental blood flow index could be calculated. Labetalol induced a significant drop of mean arterial blood pressure from 114 +/- mm Hg to 100 +/- 3 mm Hg after 30 min in this group of women. However, the uteroplacental blood flow index did not change. As we have earlier shown with this technique that uteroplacental blood flow can be severely impaired in hypertension of pregnancy, the finding of substained uteroplacental blood flow simultaneously with a decrease in blood pressure should be of clinical importance. Taken together with other studies of clinical effects, these results indicate that labetalol is useful in the treatment of hypertension of pregnancy.
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PMID:Labetalol, a combined alpha- and beta-blocker, in hypertension of pregnancy. 696 61

Hyperosmolar agents are a primary therapeutic modality employed in the treatment of traumatic intracranial hypertension. Profound hyperosmolarity accompanied by systemic dehydration is a potentially serious problem when these drugs are used repeatedly for control of intracranial pressure. Because glycerol, a water-soluble alcohol, is metabolized in the liver, its dehydrating capacity may be reduced in comparison to other agents. A series of 15 patients were treated with oral glycerol (0.5 to 1.0 gm/kg) with only minor changes in serum electrolytes, glucose, and urea nitrogen. Serum osmolarity rose from a baseline of 305 mOsm/liter to 355 mOsm/liter after 10 days of therapy. Glycerol was found to be effective and safe when employed in this protocol and proved to be a valuable adjunct to the standard methods available for control of intracranial hypertension.
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PMID:Oral glycerol for the treatment of traumatic intracranial hypertension. 705 29

This report concerns an 18-year-old boy who is hemizygote for Fabry's disease. Varying degrees of nonpulsating headache crises, lasting from a few hours to several days, began when he was 16 years of age. Painful crises in the extremities, characteristic of Fabry's disease, were not present. Although only occasional, he had several episodes of throbbing headache with vomiting without aura. The meningeal signs were equivocal, although the patient had noninfectious pleocytosis, intracranial hypertension, delayed radioisotope clearance on cisternography, and multiple old cerebral infarcts. Nonsteroidal anti-inflammatory drugs, antidepressants, carbamazepine, and glycerol were of no benefit for his headache. Although its mode of action remains obscure, prednisolone was effective for treating the headache and the aseptic meningeal reaction.
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PMID:Headache associated with aseptic meningeal reaction as clinical onset of Fabry's disease. 759 47

Neutral endopeptidase 24.11, a membrane-bound metallopeptidase, cleaves, and degrades vasoactive peptides such as atrial natriuretic peptide, endothelin, angiotensin I, substance P, and bradykinin. Therefore, the presence of this metallopeptidase may contribute to the regulation of vascular tone and local inflammatory responses in the vascular endothelium and elsewhere. We determined neutral endopeptidase in cultured human endothelial cells from different vascular beds and studied its regulation by protein kinase C. Neutral endopeptidase was detected in all cultured endothelial cell types. Lowest concentrations were measured in human endothelial cells from umbilical veins (360 +/- 14 pg/mg protein), followed by pulmonary and coronary arteries; higher concentrations were found in endothelial cells from the cardiac microcirculation (1099 +/- 73 pg/mg protein). Neutral endopeptidase content increased during cell growth but was not affected by endothelial cell growth factor or modifications of the growth medium. Stimulation of protein kinase C with 1-oleoyl-2-acetyl-rac-glycerol (0.1 to 1 mumol/L) and phorbol 12-myristate 13-acetate (0.01 to 0.1 mumol/L) induced a time- and concentration-dependent increase of endothelial cells that was inhibited by cycloheximide (5 mumol/L), an inhibitor of protein synthesis. Incubation with phospholipase C (1 mumol/L) and thrombin (10 IU/mL) induced upregulation of neutral endopeptidase, resulting in 158 +/- 26% and 150 +/- 22% increases, respectively, compared with controls. The thrombin effect was inhibited by calphostin C (1 mumol/L), an inhibitor of protein kinase C. Endothelial neutral endopeptidase is constitutively expressed in endothelial cells from different origins and is inducible by thrombin via activation of the protein kinase C pathway.
Hypertension 1995 Aug
PMID:Regulation and differential expression of neutral endopeptidase 24.11 in human endothelial cells. 763 30

Insulin-mediated vasodilation has been proposed as a determinant of in vivo insulin sensitivity. We tested whether sustained vasodilation with adenosine could overcome the muscle insulin resistance present in mildly overweight patients with essential hypertension. Using the forearm technique, we measured the response to a 40-min local intraarterial infusion of adenosine given under fasting conditions (n = 6) or superimposed on a euglycemic insulin clamp (n = 8). In the fasting state, adenosine-induced vasodilation (forearm blood flow from 2.6 +/- 0.6 to 6.0 +/- 1.2 ml min-1dl-1, P < 0.001) was associated with a 45% rise in muscle oxygen consumption (5.9 +/- 1.0 vs 8.6 +/- 1.7 mumol min-1dl-1, P < 0.05), and a doubling of forearm glucose uptake (0.47 +/- 0.15 to 1.01 +/- 0.28 mumol min-1dl-1, P < 0.05). The latter effect remained significant also when expressed as a ratio to concomitant oxygen balance (0.08 +/- 0.03 vs 0.13 +/- 0.04 mumol mumol-1, P < 0.05), whereas for all other metabolites (lactate, pyruvate, FFA, glycerol, citrate, and beta-hydroxybutyrate) this ratio remained unchanged. During euglycemic hyperinsulinemia, whole-body glucose disposal was stimulated (to 19 +/- 3 mumol min-1kg-1), but forearm blood flow did not increase significantly above baseline (2.9 +/- 0.2 vs 3.1 +/- 0.2 ml min-1dl-1, P = NS). Forearm oxygen balance increased (by 30%, P < 0.05) and forearm glucose uptake rose fourfold (from 0.5 to 2.3 mumol min-1dl-1, P < 0.05). Superimposing an adenosine infusion into one forearm resulted in a 100% increase in blood flow (from 2.9 +/- 0.2 to 6.1 +/- 0.9 ml min-1dl-1, P < 0.001); there was, however, no further stimulation of oxygen or glucose uptake compared with the control forearm. During the clamp, the ratio of glucose to oxygen uptake was similar in the control and in the infused forearms (0.27 +/- 0.11 and 0.23 +/- 0.09, respectively), and was not altered by adenosine (0.31 +/- 0.9 and 0.29 +/- 0.10). We conclude that in insulin-re15-76sistant patients with hypertension, adenosine-induced vasodilation recruits oxidative muscle tissues and exerts a modest, direct metabolic effect to promote muscle glucose uptake in the fasting state. Despite these effects, however, adenosine does not overcome muscle insulin resistance.
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PMID:Insulin resistance and vasodilation in essential hypertension. Studies with adenosine. 792 33


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