Glycerol and dextran combined in the therapy of acute stroke. A placebo-controlled, double-blind trial with a planned interim analysis.

Frei, Anja; Cottier, Christopher; Wunderlich, P; Ludin, Edward N.

doi:10.1161/01.str.18.2.373

Cited by 34 publications

(31 citation statements)

References 46 publications

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“…26 Japanese clinicians have infused such mixtures into patients very rapidly, apparently without ill effect. 27 Following our preliminary experience, special care was taken to avoid excessive infusion rates; it was gratifying that after 7 days, the mean reduction of hemoglobin concentration in patients receiving glycerol in our study was much smaller (about Vi) than that reported by Frei et al 25 Indeed, following 6 days of glycerol or placebo treatment, mean reductions encountered in our patients were 0.54 and 0.12 g/dl, respectively; the difference of only 0.4 g/dl was statistically but not clinically significant (Table 5). Furthermore, such subclinical reductions in hemoglobin concentration after infusion of glycerol in saline may be attributed to a While our overall results show no clinically or statistically significant difference in outcome between patients treated with glycerol or saline, there were too few comatose and semicomatose patients to make any kind of reliable independent estimate of the effect of treatment within these strata.…”

Section: Resultssupporting

confidence: 47%

“…16 Discussion Hitherto, studies purporting to evaluate the possible beneficial effect of intravenous glycerol in patients with acute stroke have yielded contradictory and inconclusive results. 17 " 25 Commonly, there was no attempt to distinguish hemorrhagic from ischemic episodes (especially in earlier trials), and if attempted, objective confirmation of the diagnosis with CT was lacking or inconsistent.…”

Section: Resultsmentioning

confidence: 99%

“…17 " 24 The study by Frei et al, 25 in which pretreatment CT was performed on all patients, concerned ischemic stroke. Other important shortcomings in the design and execution of these investigations included failure to stratify patients according to stroke severity (anticipated prognosis), prolonged delays before initiating treatment, limited measures of outcome, exclusion of the most severely affected patients, too few patients, and insufficient period of follow-up.…”

Section: Resultsmentioning

confidence: 99%

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Treatment of acute cerebral hemorrhage with intravenous glycerol. A double-blind, placebo-controlled, randomized trial.

Kumana

Lauder

et al. 1992

Stroke

124

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Background and Purpose: Hitherto, treatment of acute cerebral hemorrhage with intravenous glycerol has not been evaluated in rigorous clinical studies with sufficient patient numbers.Methods: We undertook a double-blind, stratified and randomized, placebo-controlled clinical trial. Only patients with a first stroke admitted to the hospital within 24 hours after onset of symptoms were recruited, provided computed tomography confirmed hemorrhage and informed consent was obtained. After stratification into alert, semicoma, and coma subgroups using the Glasgow Coma Scale, 107 patients received active treatment (500 ml of 10% glycerol in saline by intravenous infusion over 4 hours on 6 consecutive days) and 109 were given corresponding saline treatment. Using a variety of objective scoring systems, patients were followed up for up to 6 months.Results: At follow-up, all measures of outcome in the treated and control groups were very similar. At 6 months, respective mortality rates were 37 of 107 and 33 of 109. Corresponding mean±SD improvements in Scandinavian Stroke Study Group scores were 8.35±16.9 versus 11.55±15.6 (long-term) and 0.64±7.3 versus 2.40±6.9 (prognostic), and improvements in the Barthel Index ratings were 10.72±24.7 versus 13.95 ±23.3, respectively. Glasgow Coma Scale score improvements in the survivors were 0.81 ±1.5 and 1.16±1.7 in the treated and control groups, respectively. Hemolysis (generally subclinical) was the only adverse effect of glycerol noted.Conclusions: In the absence of any clinically or statistically significant difference in outcome between the treated and control groups, this trial provides no justification for glycerol therapy following acute cerebral hemorrhage. (Stroke 1992;23:967-971) KEY WORDS • cerebral hemorrhage • clinical trials • glycerin

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Section: Resultssupporting

confidence: 47%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Treatment of acute cerebral hemorrhage with intravenous glycerol. A double-blind, placebo-controlled, randomized trial.

Kumana

Lauder

et al. 1992

Stroke

124

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“…Primary mixed glial cells were prepared from 1 -3-day-old postnatal Sprague-Dawley rat pups, as described previously (33). Briefly, the brain cortices were pretreated in 0.25% trypsin solution containing of 1 mM EDTA and 1% papain for 5 min in a 37°C incubator, passed through a nylon mesh (100 μm), and plated at 2 × 10 5 cells /cm 2 in 0.01% poly-D-lysine-coated T-75 flasks.…”

Section: Cell Culturesmentioning

confidence: 99%

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

et al. 2009

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Abstract. The roots of Panax notoginseng (PN) are commonly used as a therapeutic agent to stop hemorrhage and as a tonic to promote health in traditional Korean medicine. Stroke triggers an inflammatory response that not only plays a central role in the pathogenesis of cerebral ischemia, but also induces secondary damage. This study was designed to investigate the neuroprotective effects of the methanol extract of PN on the infarct volume induced by middle cerebral artery occlusion (MCAO) (90-min occlusion and 24-h reperfusion) in rat brains. The PN extract (50 mg/ kg, i.p.) was administered 2 h after the onset of MCAO. The PN-treated groups had a reduction in infarct volume by 23.82 ± 8.9%. In the PN extract-treated groups, the microglial density was significantly decreased in the peri-infarct region; the underlying mechanism was inhibition of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, via blocking of the NF-κB pathway. Furthermore, in vitro studies showed that the PN extract significantly reduced the production of iNOS-derived NO and COX-2-derived prostaglandin E 2 through the regulation of gene transcription levels in primary microglia and BV-2 cells. These results suggest that anti-inflammatory and microglial activation inhibitory effects of the PN extract may contribute to its neuroprotective effects in brain ischemia.

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“…With the large doses of steroids which have been used, infective complications and elevation of plasma glucose or exacerbation of diabetes are frequent (Poungvarin et al, 1987). Despite many studies with intravenous glycerol there is no consensus on its effect on stroke (Bayer et al, 1987;Fawer et al, 1978;Frei et al, 1987;Gilsanz et al, 1975;Larsson et al, 1976;Mathew et al, 1972;Meyer et al, 1975). In an overview of the published trials, Sandercock (1987) concluded that the 6 week mortality in stroke patients after glycerol may fall by 36% compared with placebo, but that the 95% confidence limits for this improvement range from 4%-58%.…”

Section: Anti-oedema and Other Agentsmentioning

confidence: 99%

Therapeutic interventions in acute stroke.

Lees

1992

Brit J Clinical Pharma

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1. Potential therapies for ischaemic stroke include agents to reduce oedema, to improve cerebral perfusion, to reduce excitotoxic damage, to minimise free‐radical induced injury and to reduce complications such as deep venous thrombosis. 2. Of the anti‐oedema drugs, steroids are ineffective and possibly dangerous; intravenous glycerol is unproven. 3. Haemodilution to reduce whole blood viscosity and improve perfusion is ineffective. Thrombolytic drugs have not been adequately tested but several randomised multicentre trials are now commencing. Early treatment and CT scanning are essential. 4. Anticoagulants and antiplatelet drugs may have wide applicability but have not been tested in the acute phase of stroke. A multi‐centre trial will address this issue. 5. Neuronal cytoprotection offers exciting prospects for acute stroke treatment. Antagonists of glutamate at the NMDA receptor, calcium and sodium channel blocking agents and free radical scavenging drugs have potent effects experimentally. Several agents are now reaching clinical trials. The calcium antagonist nimodipine has been disappointing in large scale trials but some studies were flawed by late treatment. 6. Successful treatment of acute stroke is likely to combine several approaches. 7. Therapeutic trials in stroke must include CT scanning, early treatment and a multicentre approach to achieve large numbers of patients.

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Glycerol and dextran combined in the therapy of acute stroke. A placebo-controlled, double-blind trial with a planned interim analysis.

Cited by 34 publications

References 46 publications

Treatment of acute cerebral hemorrhage with intravenous glycerol. A double-blind, placebo-controlled, randomized trial.

Treatment of acute cerebral hemorrhage with intravenous glycerol. A double-blind, placebo-controlled, randomized trial.

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

Therapeutic interventions in acute stroke.

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