Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transitive cerebral distension which is necessary for the neuro-surgeon during interventions is obtained by moderate controlled hyperventilation, deliberate arterial hypotension, application of the anti-sludge therapy for the cerebral microcirculation. Only the initial mannitol dose applied is useful for the subject with intra-cranial hypertension. Mannitol is not active in cases with cerebral oedema due to severe cerebral contusion. In such cases corticoids are the major therapeutic indication. The anti-sludge effects of mega-doses of thiamine in cases with severe disturbances in the microcirculation of basal nuclei and profound comatose conditions, makes possible to apply therapeutic dehydration and is associated with an increase in the resistance of the cerebral tissue to hypoxia. Volatile anesthetic agents increase the intra-cranial pressure in patients with expanding intra-cranial processes. Thiamine neuroleptanalgesia and synaptanalgesia, with or without xylocaine potentiation, have resulted in a satisfactory cerebral distension. Controlled hypotension and increased pressure are, for the time being, just a prospective field.
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PMID:[Current management of anesthesia and intensive therapy of expansive processes with intracranial hypertension]. 13 8

Three cases of pseudocysts following surgery and chemotherapy for glioblastomas are reported. Their clinical picture was similar, consisting of intracranial hypertension without primary modification of focal signs. CT scanning has been able to detect the cystic aspect and to eliminate a true tumour recurrence. Medical treatment (steroids or Mannitol) seems inefficient. Evacuation of the cyst is the only efficient method of treatment.
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PMID:Cerebral pseudocysts following chemotherapy of glioblastomas. 20 72

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

To evaluate the effects of mannitol on aqueous flare (aqueous protein concentration), we administered an intravenous clinical therapeutic dose to normal young adults (average age 20.1 years), to normal older adults (average age 61.5 years), and also to patients with diabetes mellitus, systemic hypertension, or pseudoexfoliation syndrome who were about to undergo intraocular surgery (average age 66.4 years). Protein and cell levels in the aqueous were determined with a device that measures laser light scatter in the aqueous. Mannitol increased the intensity of aqueous flare. In all subjects, the intensity of aqueous flare was greatest around 1 h following drug administration; the magnitude and duration of the aqueous flare increase were significantly greater in normal older adults than in normal young adults; the magnitude was essentially the same in older adults with and without disease. The effect reversed within 6 h of drug administration in normal subjects. We consider the findings to represent changes in actual aqueous protein concentration and discuss the possible causes of this phenomenon.
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PMID:Increased aqueous flare as a result of a therapeutic dose of mannitol in humans. 157 89

In recent years the treatment of bacterial meningitis has been modified on the basis of a better understanding of its physiopathological mechanisms. It has been shown, for example, that the inflammatory reaction is the primary cause of brain damage in bacterial meningitis. Inflammation and consequent brain damage are greatest in the first hours of antibiotic treatment when rapid and massive bacteriolysis takes place. In effect, the bacterial components activate metabolic pathways and cellular elements leading to the release of inflammation mediators: cytokines (TNF, IL-I) neutrophil degranulation products, complement components and clotting factors. Initially these substances make the blood-fluid and blood-brain barriers permeable. The result is cerebral oedema, excessive fluid pressure, congestion of the cerebral blood vessels and finally endocranial hypertension, reduced cerebral flow, cerebral hypoxia and brain damage. This sequence of events can be stopped by a multifactorial therapy that is not only aetiological (antibiotic) but also treats the inflammation, oedema (Dexamethasone, Mannitol) and symptoms. In this study 129 patients with non-tubercular bacterial meningitis were treated as described. All patients were administered Ceftriaxone (100 mg/kg per diem) Dexamethasone (0.2-0.3 mg/kg/per diem), Mannitol, fluid restriction and--where necessary--intensive symptomatic therapy (against shock, convulsions, fever). Both the antibiotic and the corticosteroid were also administered intrathecally at the time of the first lumbar puncture at intake. Of these 129 patients, 7 died very soon after admission as they had arrived in a moribund condition. Duration of therapy was 3-6 days in 90% of these cases. There were no recurrences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rational basis of modern therapy of bacterial meningitis. Review of the literature and our clinical experience of 122 pediatric cases. 180 76

The effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and EEG monitored by Cerebral Function Monitor (CFM) were compared after bolus administration of mannitol (n = 55) and thiopentone (n = 67) to control intracranial hypertension in 18 severely head injured patients. Mannitol increased CPP in 89% of occasions and thiopentone in only 54% (p < 0.001). Thiopentone caused a mean increase in CPP +0.6 kPa (+5.0 +/- 1.6 mmHg) when the minimum pre-bolus voltage of CFM was above 4 microV and a fall in CPP -0.5 kPa (-4.1 +/- 1.6 mmHg) when cortical electrical activity was already severely depressed (p < 0.0002). When pre-bolus CFM was below 4 microV mannitol was superior to thiopentone. This different effect on CPP was due to a significantly greater fall in mean arterial pressure in the thiopentone sub-group -1.6 versus -0.3 kPa (-12.4 +/- 1.5 mmHg, -2.8 +/- 1.2 mmHg; p < 0.001). Severe and unpredictable hypotension occurred, particularly in the thiopentone low CFM sub-group. This symptomatic therapy seems inadequate but a targeted treatment of intracranial hypertension could be possible only with a more sophisticated monitoring, including continuous data on cerebral blood flow and adequacy to metabolic demand.
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PMID:Effects of thiopentone and mannitol on cerebral perfusion pressure and E.E.G. in head injured patients with intracranial hypertension. 184 98

Renal arteriography with concomitant renal vein renin profiling remains the diagnostic standard for evaluating the anatomic and physiologic significance of stenotic renal artery lesions in hypertensive patients. False-negative renal vein renin profiles with failure of lateralization in patients with anatomically apparent high-grade stenosis complicate the diagnostic process. Mannitol is frequently administered prophylactically to minimize the risk of dye nephropathy in these patients. Yet, the potential effects of mannitol on renal vein renin profiling in man have not been previously reported. Seven patients with renovascular hypertension were studied prospectively to determine changes in renal vein renin profiles before and after mannitol prophylaxis. Despite captopril stimulation, all patients demonstrated significant renin suppression leading to the loss of renin lateralization in patients with unilateral renovascular hypertension. In 60% of the patients, renal vein renin ratios fell to below the standard 1.5 to 1 ratio after mannitol infusion. In patients with bilateral renovascular disease, the least stenotic side suppressed completely, while the more stenotic side suppressed partially. Percent suppression analysis showed a mean suppression of 56.8% on the stenotic side versus 8.2% on the noninvolved side (P less than 0.002). In every study, suppression equaled or exceeded 32% on the involved side and was less than this on the noninvolved side. Thus, the degree of renin suppression following mannitol infusion may prove to be an important tool in the diagnosis of clinically significant stenotic lesions. The mechanism of mannitol-induced suppression remains undefined, but appears independent of volume expansions or dilutional effects. The inhibitory effects of mannitol on renin profiles can obscure the diagnosis of underlying renovascular hypertension.
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PMID:Suppression of renal vein renin profiles by mannitol prophylaxis: implications in the evaluation of renovascular hypertension. 196 48

Mannitol is widely used to reduce intracranial pressure and is protective against ischemic and nephrotoxic acute renal failure. However, the capacity of this seemingly innocuous agent to produce acute renal failure is not well recognized. We report herein the clinical course of 8 cases of mannitol-induced acute renal failure. In addition, we reviewed all previously reported cases of mannitol-induced renal failure. In the present series, acute oliguric renal failure developed within 3.5 +/- 1.1 (mean +/- SD) days after receiving daily and total mannitol doses of 189 +/- 64 g and 626 +/- 270 g, respectively, over 3.5 +/- 1.5 days. The peak serum creatinine was 5.7 +/- 2.7 mg/dl and peak osmolal gap was 74 +/- 39 mOsm/kg water. Renal tubular epithelial cells containing vacuoles were seen in the urinary sediments of 6 patients. Renal function improved rapidly upon discontinuation of mannitol and/or removal of mannitol by hemodialysis. In those previously reported cases in which the baseline renal function was normal, acute renal failure developed after receiving total mannitol doses of 1171 +/- 376 g. The peak osmolal gap was 107 +/- 17. In contrast, in those with underlying renal compromise, renal function worsened after a total mannitol dose of 295 +/- 143 g. The pathogenesis of mannitol-induced renal failure is not yet established but may be associated with renal vasoconstriction produced by high concentrations of mannitol. This may be averted in clinical practice by monitoring the osmolal gap, rather than serum osmolality alone, when using mannitol infusions for the treatment of intracranial hypertension.
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PMID:Mannitol-induced acute renal failure. 211 70

CBF and ICP were measured in cats following cerebral cold injury and mannitol infusion. Mannitol was found to reduce the intracranial hypertension caused by the injury. The restoration of CBF and ICP was of short duration and was followed by a reduction of CBF and elevation of ICP. A repeated restoration of CBF by a second dose of mannitol was followed by a more severe impairment of CBF. The prolonged beneficial effect of mannitol on CBF after brain injury has to be reassessed.
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PMID:Transient effect on mannitol on cerebral blood flow following brain injury. 212 73

To evaluate the effects of mannitol on aqueous flare (aqueous protein concentration), we administered an intravenous clinical therapeutic dose to normal young adults (average age, 20.1 years), to normal older adults (average age, 61.3 years), and also to patients with diabetes mellitus, systemic hypertension, or pseudoexfoliation syndrome who were about to undergo intraocular surgery (average age, 66.4 years). Protein and cell levels in the aqueous fluid were determined with a device that measures laser light scattering in the aqueous fluid. Mannitol increased aqueous flare intensity. In all subjects, aqueous flare intensity was greatest around one hour following drug administration; the magnitude and the duration of the aqueous flare increase were significantly greater in normal older subject than in normal young adults; the magnitude was essentially the same in older adults with and without diseased barrier. The effect was reversed within 6 hours of drug administration in normal subjects. We considered the findings to represent changes in actual aqueous protein concentration and discussed the possible causes of this phenomenon.
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PMID:[Increase in aqueous flare by a therapeutic dose of mannitol in humans]. 251 89


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