rutin has been researched along with Ischemia* in 5 studies
2 trial(s) available for rutin and Ischemia
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The effect of hydroxyethylrutoside and its combination with acetylsalicylic acid in patients with obliterative atherosclerosis.
The effect of 7-mono-hydroxyethylrutoside and its combination with acetylsalicylic acid was evaluated in a controlled clinical trial, performed in 105 patients with obliterative atherosclerosis of the lower limbs, and using non-invasive measurement of peripheral haemodynamic parameters--blood flow during reactive hyperaemia and ankle systolic blood pressure. Patients, randomized into three groups, received either placebo or 7-mono-hydroxyethylrutoside alone or in combination with acetylsalicylic acid for 12 months. The placebo group showed a decrease in maximum calf blood flow and a decrease in ankle systolic pressure. Administration of 7-mono-hydroxyethylrutoside did not lead to any significant changes in systolic pressure but there was a decrease in the maximum calf blood flow. There were no statistically significant changes in patients receiving the 7-mono-hydroxyethylrutoside and acetylsalicylic acid combination who, by contrast, showed a tendency to increased values of the parameters measured. Topics: Adult; Analgesics; Anticoagulants; Arteriosclerosis Obliterans; Aspirin; Clinical Trials as Topic; Drug Therapy, Combination; Female; Hemodynamics; Humans; Hydroxyethylrutoside; Ischemia; Leg; Male; Middle Aged; Plethysmography; Rutin | 1989 |
[Benzopyrone in the therapy of postreconstructive edema. A clinical double-blind study].
Topics: Adult; Aged; Coumarins; Double-Blind Method; Drug Combinations; Female; Humans; Hydroxyethylrutoside; Ischemia; Leg; Lymphedema; Male; Middle Aged; Postoperative Complications; Rutin | 1985 |
3 other study(ies) available for rutin and Ischemia
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Troxerutin Abrogates Ischemic/Reperfusion-Induced Brain Injury through Ameliorating Oxidative Stress and Neuronal Inflammation by Inhibiting the Expression of NLRP3 in Sprague Dawley Rats.
Cerebral ischemic reperfusion (I/R) infarction is mostly associated with serious brain injury, cognitive damage, and neurological deficits. The oxidative stress mechanisms in the neurological region lead to higher reactive oxygen species production followed by oxidative stress, inflammation of neurons, and death of brain cells. The current work aims to evaluate the effect of troxerutin (TXN) on cerebral injury stimulated by I/R-induced ischemic stroke and examines the mechanistic effect of TXN on neuroinflammation in the Sprague Dawley model. The experimental rats were randomized in to four groups: (i) sham control, (ii) I/R + vehicle, (iii) I/R + 10 mg/kg bw TXN, and (iv) I/R + 20 mg/kg bw TXN. In the TXN administration and control, groups were injected intraperitoneally 15 min before reperfusion and every day for 7 days, except the sham group. Orally administered TXN (10 and 20 mg/kg/bw) modulated the water content, lowered the infarct volume, and abrogated score defects of neuron and changes in the brain tissue sample. In our study, the TXN-stimulated cerebral injury exhibited leakage of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) of the neuronal sample of tissues and showed higher antioxidant enzymes superoxide dismutase, catalase, the oxidized form of glutathione peroxidase, and the reduced form of glutathione levels. This biochemical result was additionally proved by histopathological assessment. Changes were made in antioxidant and inflammatory markers expressions interleukin-6 (IL-6), IL-4, IL-10, vascular endothelial growth factor, and cerebral induced rats. The overall findings showed that TXN protected the brain tissues from neuroinflammatory oxidative stress by reducing cerebral injury in Sprague Dawley rats. Further, the messenger RNA expression of cerebral I/R-induced animal tissues down-regulated NLRP3, caspase-1, tumor necrosis factor-α, ASC, IL-1β, and Toll-like receptor 3 (TLR3). Therefore, the TXN action on TLR3 induced brain stroke is an excellent therapeutic approach for brain damage. Topics: Animals; Anticoagulants; Dose-Response Relationship, Drug; Gene Expression Regulation, Neoplastic; Hydroxyethylrutoside; Ischemia; Neuroinflammatory Diseases; Neurons; NLR Family, Pyrin Domain-Containing 3 Protein; Oxidative Stress; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury | 2021 |
Intravenous hydroxyethylrutosides combined with long-term oral anticoagulation in atherosclerotic nonreconstructable critical leg ischemia: a retrospective study.
To evaluate in a group of seriously diseased patients with nonreconstructable chronic critical leg ischemia (CLI), treated by a combination of i.v. hydroxyethylrutosides (HR)* and oral anticoagulation (AC) by warfarin, the short-term effects on the cutaneous microvascular blood perfusion of the soles of feet and especially the long-term clinical outcome in terms of amputation and death.. A retrospective comparison between two groups of patients, HR + AC and a comparable reference group, fulfilling the same inclusion and exclusion criteria corresponding to the definition of CLI according to the Second European Consensus Document (1991). Clinical follow-up in both groups was made after 1, 3, 6, 12, and 24 months.. Patients were examined at university departments of clinical physiology with special interest in peripheral vascular disease, in cooperation with colleagues at university departments of surgery, internal medicine and dermatology of Karolinska Hospital, Södersjukhuset and Huddinge Hospital.. A total of seventy patients with CLI according to the definition of the Second European Consensus Document, 1991, ie, besides severe rest pain or ischemic lesions also a toe blood pressure < 30 mg Hg. Group with HR + anticoagulation (AC): 42 patients (19 diabetics, 23 nondiabetics). Reference group: 28 patients (18 diabetics, 10 nondiabetics). For distribution of age and toe blood pressure at baseline, see Table I.. Therapy group: besides ordinary standard therapy, daily HR infusions for a mean period of 3.6 weeks + oral anticoagulation continued to the end of the study at 24 months. A comparable reference group on the same basic therapy but without the combination HR + AC. PARAMETERS IN EVALUATION: Short-term parameters: clinical data, skin temperature, and fluorescein imaging. Long-term outcome: amputation or death.. Short-term and long-term results with HR + AC indicated that patients with severe CLI and very poor prognosis benefited in terms of survival and limb salvage from initial therapy with HR infusion combined with long-term oral anticoagulation. Results of this combined treatment seem at least comparable with those with i.v. prostacyclin analogies. Topics: Administration, Oral; Aged; Amputation, Surgical; Anticoagulants; Arteriosclerosis; Blood Pressure; Cardiovascular Agents; Contrast Media; Diabetic Angiopathies; Drug Therapy, Combination; Fluorescein; Follow-Up Studies; Foot; Humans; Hydroxyethylrutoside; Infusions, Intravenous; Ischemia; Leg; Longitudinal Studies; Microcirculation; Prognosis; Retrospective Studies; Skin Temperature; Survival Rate; Treatment Outcome; Warfarin | 1999 |
The effect of O-(beta-hydroxyethyl)-rutosides on function and structure of the ganglion cells.
The effect of O-(beta-hydroxyethyl)-rutosides (Venoruton) on function and structure of the motor anterior-horn cells of the lumbar spinal cord was investigated under conditions of ischemia in the rabbit. The determination of the functional parameters of the ganglion cells, such as maximal function time (Fm), disappearance time (SFm), relative efficiency (La), and regeneration expenditure (Ea) revealed that 50 mg/kg of Venoruton injected prior to repeated aortic occlusion of short duration (occlusion time A = Fm and A = 2 Fm, respectively) caused the efficiency of the anterior-horn cells to be decreased. Both qualitative and quantitative analysis of the mitochondrial structure after prolonged aortic occlusion (15-25 min) revealed that after prior injection of Venoruton irreversible structural changes in the mitochondrial membranes of the ischemic area in the spinal cord occurred after aortic occlusion of 15 min duration. In the untreated controls such changes were not observed before 20 min of occlusion. The mitochondrial structure of the non-ischemic area in the spinal cord was found to be undamaged, however, in both controls and experimental animals. Venoruton given after prolonged aortic occlusion resulted in less pronounced structural changes of the mitochondria in the ischemic area of the experimental animals than those found in the untreated controls; paralysis of the hind extremities was found to occur only after prolonged occlusion (25 min), whereas in the controls such changes were already observed after 20 min of occlusion. Since no ultrastructural changes in the ganglion cells of the non-ischemic area in the in the lumbar spinal cord were observed after application of Venoruton, it is assumed that the decreased efficiency of the motor anterior-horn cells found in the ischemic area when Venoruton had been injected before the aortic occlusion may be due to reactions of the cell that only occur when the blood supply has been completely cut off and Venoruton is present at the same time. Topics: Animals; Anterior Horn Cells; Female; Hydroxyethylrutoside; Ischemia; Male; Mitochondria; Rabbits; Reflex, Monosynaptic; Rutin; Spinal Cord | 1976 |