heparitin-sulfate has been researched along with Ischemic-Attack--Transient* in 5 studies
1 trial(s) available for heparitin-sulfate and Ischemic-Attack--Transient
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[Comparative study of ASA and heparan sulfate in the secondary prevention of cerebrovascular disorders].
Aim of our study was to compare heparan sulphate and acetylsalicylic acid (ASA) in the secondary prevention of cerebrovascular events. Eighty patients with recent episodes of RIA or minor stroke of atherothrombotic origin were randomized in two groups of 40, one treated with heparan sulphate and the other with ASA. The two groups were homogeneous for age, sex, clinical history and type of events qualifying for enrollment. After a 6-month follow-up no difference was found in fatal or non fatal vascular events. The incidence of adverse reactions was significantly lower in the heparan sulphate group. All the patients showed a trend towards improvement in cognitive functioning, but a significant improvement in attentional functions was observed only in the heparan sulphate group. As hypothesis, it may be supposed that such clinical results depend on a better perfusion of inner watershed cerebral areas. Topics: Aged; Aged, 80 and over; Aspirin; Cerebrovascular Disorders; Female; Fibrinolytic Agents; Follow-Up Studies; Heparitin Sulfate; Humans; Ischemic Attack, Transient; Male | 1993 |
4 other study(ies) available for heparitin-sulfate and Ischemic-Attack--Transient
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Vascular Endothelial Growth Factor 165-Binding Heparan Sulfate Promotes Functional Recovery From Cerebral Ischemia.
Although VEGF. Both rat brain endothelial cell line 4 and primary rat neural progenitor cells were used to evaluate the potential angiogenic and neurogenic effects of HS7 in vitro. For in vivo experiments, male Sprague-Dawley rats were subjected to 100 minutes of transient focal cerebral ischemia, then treated after 4 days with either PBS or HS7. One week later, infarct volume, behavioral sequelae, immunohistochemical markers of angiogenesis and neural stem cell proliferation were assessed.. A VEGF-activating glycosaminoglycan sugar, by itself, is able to enhance endogenous VEGF Topics: Animals; Blood-Brain Barrier; Brain Ischemia; Cell Proliferation; Heparitin Sulfate; Infarction, Middle Cerebral Artery; Injections, Intraventricular; Ischemic Attack, Transient; Male; Neovascularization, Physiologic; Neural Stem Cells; Rats; Rats, Sprague-Dawley; Recovery of Function; Stroke; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2 | 2020 |
Early recovery after cerebral ischemia risk of subsequent neurological deterioration.
Given the high short-term risk of stroke after transient ischemic attack, we hypothesized that substantial acute neurological recovery in patients presenting with cerebral ischemia would be associated with a greater risk of subsequent neurological deterioration due to recurrent cerebral ischemia. Data from the Trial of ORG10172 in Acute Stroke Treatment, a randomized trial of the heparinoid danaparoid, were analyzed to determine whether substantial acute recovery, defined as an improvement of greater than or equal to 75% on National Institutes of Health Stroke Scale (NIHSS) between baseline and 24 hours, was associated with a greater risk of subsequent deterioration, defined as a worsening on the NIHSS between day 1 and day 90. Of 1,184 subjects meeting entry criteria, 63 (5.3%) had substantial acute recovery. Subsequent deterioration was more common in those with substantial acute recovery compared with others (48 vs 33%; p = 0.028 by Fisher's exact test). In multivariable models, substantial acute recovery remained an independent predictor of subsequent deterioration (odds ratio, 3.0; 95% confidence interval, 1.7-5.2; p < 0.001). Among patients with acute cerebral ischemia, those who recover substantially within 24 hours may be at greater risk of subsequent neurological deterioration due to causes other than hemorrhage. Topics: Aged; Anticoagulants; Blood Glucose; Blood Pressure; Case-Control Studies; Chondroitin Sulfates; Dermatan Sulfate; Disease Progression; Drug Combinations; Female; Follow-Up Studies; Heart Rate; Heparitin Sulfate; Humans; Ischemic Attack, Transient; Male; Middle Aged; Nervous System Diseases; Neurologic Examination; Odds Ratio; Randomized Controlled Trials as Topic; Recovery of Function; Risk; Time Factors | 2003 |
Reduction of brain injury using heparin to inhibit leukocyte accumulation in a rat model of transient focal cerebral ischemia. I. Protective mechanism.
Heparin has long been established as an anticoagulant. Although heparin has been demonstrated to reduce brain injury after ischemia and reperfusion, its mechanism of action remains unknown. Recent investigations reveal that it can modulate biological processes such as binding to adhesion receptors on endothelial cells and leukocytes. The authors hypothesized that heparin's protective effect is closely related to its antileukocyte adherence property. They evaluated the efficacy of sulfated polysaccharides (unfractionated heparin, low-molecular-weight heparin, heparan sulfate, chondroitin sulfate C, and dextran sulfate) on leukocyte accumulation, infarction size, and neurological outcome after transient focal cerebral ischemia in rats subjected to 1 hour of ischemia and 48 hours of reperfusion. Forty-nine animals were included in the study. The animals receiving unfractionated heparin or dextran sulfate showed a significant reduction in leukocyte accumulation, infarct size, and neurological dysfunction 48 hours after reperfusion (p < 0.05) when compared to untreated animals. The animals receiving unfractionated heparin also showed significantly better results than the animals receiving an equivalent anticoagulant dose of low-molecular-weight heparin. These data indicate that heparin's antileukocyte property plays a more important role than its anticoagulant ability in neuronal protection. The relative potency of the sulfated polysaccharides tested in leukocyte depletion was closely related to their degree of sulfation. Thus, in addition to demonstrating the potential efficacy of heparin as a therapeutic agent for ischemia and reperfusion injury by the prevention of leukocyte accumulation, the results also serve as a basis for studying important cellular and molecular events that contribute to tissue damage. Topics: Animals; Cell Adhesion; Chondroitin Sulfates; Dextran Sulfate; Heparin; Heparitin Sulfate; Ischemic Attack, Transient; Leukocytes; Male; Peroxidase; Rats; Rats, Sprague-Dawley; Reperfusion Injury | 1996 |
Venous occlusion test for the release of heparan sulfate from endothelium.
Topics: Adult; Constriction; Diabetes Mellitus, Type 1; Endothelium, Vascular; Female; Heparitin Sulfate; Humans; Ischemic Attack, Transient; Male; Neoplasms; Veins | 1993 |