Therapeutic effects of hydroxysafflor yellow A on focal cerebral ischemic injury in rats and its primary mechanisms
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The therapeutic effects of hydroxysafflor yellow A (HSYA), extracted from Carthamus tinctorius. L, on focal cerebral ischemic injury in rats and its related mechanisms have been investigated. Focal cerebral ischemia in rats were made by inserting a monofilament suture into internal carotid artery to block the origin of the middle cerebral artery and administrated by HSYA via sublingular vein injection in doses of 1.5, 3.0, 6.0 mg kg(-1) at 30 min after the onset of ischemia, in comparison with the potency of nimodipine at a dose of 0.2 mg kg(-1). Then, 24 h later, the evaluation for neurological deficit scores of the rats were recorded and postmortem infarct areas determined by quantitative image analysis. At the end of the experiment, blood samples were taken to determine plasma 6-Keto-PGF1alpha/TXB2 by radioimmunoassays and blood rheological parameters. The effects exerted by HSYA on thrombosis formation by artery vein by-pass method and ADP-induced platelet aggregation in vivo and in vitro were investigated, respectively. The results indicated that more than 30% of the area of ischemic cerebrum was observed in the ischemic model group. HSYA dose-dependently improved the neurological deficit scores and reduced the cerebral infarct area, and HSYA bore a similarity in potency of the therapeutic effects on focal cerebral ischemia to nimodipine. The inhibition rates of thrombosis formation by HSYA at the designated doses were 20.3%, 43.6% and 54.2%, respectively, compared with saline-treated group. Inhibitory activities of HSYA were observed on ADP-induced platelets aggregation in a dose-dependent manner, and the maximum inhibitory aggregation rate of HSYA was 41.8%. HSYA provided a suppressive effect on production of TXA2 without significant effect on plasma PGI2 concentrations. Blood rheological parameters were markedly improved by HSYA, such as whole blood viscosity (from 21.71 +/- 4.77 to 11.61 +/- 0.90 mPa.s), plasma viscosity (from 2.73 +/- 0.53 to 1.42 +/- 0.07 mPa.s), deformability (from 0.66 +/- 0.26 to 0.77 +/- 0.33) and aggregation of erythrocyte (from 3.24 +/- 0.41 to 2.57 +/- 0.30), but no significant effect of HSYA on homatocrit was found (from 51.38 +/- 4.68% to 49.91 +/- 2.32%). HSYA appears to be a good potential agent to treat focal cerebral ischemia, and the underlying mechanisms exerted by HSYA might be involved in its inhibitory effects on thrombosis formation and platelet aggregation as well as its beneficial action on regulation of PGI2/TXA2 and blood rheological changes in rats.Keywords:
Nimodipine
Objective: To study the differences of the protective role between pre-treated and treated after ischemia onset with Nimodipine on the neurons in cerebral ischemia areas. Methods:The cerebral ischemic model of rat was made by occluding left middle cerebral artery according to Nagasawy and Zea Longa improvement method. The rats were pre-treated, treaded after ischemia onset or pre-treated plus treaded after ischemia with Nimodipine. The percentage of the infarction volume was calculated by red tetrazoline (ITC) pigmentation. The level of Caspase-3 and Bcl-2 mRNA were measured by RT-PCR method. Results: The percentage of the cerebral infarction volume of pre-treated, treated after ischemia and pre-treated plus treaded after ischemia with Nimodipine was significant lower than that of control, and in the above three groups, the infarction percentage of the last group was lower than the anterior two. However, there was no significant difference between the percentage of pre-treated group and the one of treated after ischemia. The level of Caspase-3 mRNA was the highest in control group, and the expression was lower in treated after ischemia group, pre-treated group and pre-treated plus treated after ischemia group in turn. The level of Bcl-2 mRNA was reversed in the four groups. Conclusion: There was stronger protective effects of pre-treated plus treated after ischemia with Nimodipine than pre-treated or treated after ischemia.
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OBJECTIVE To evaluate the therapeutic effect of nimodipine on mild/medium Vascular dementia.METHODS Thirty-five patients with Vascular dementia were treated with nimodipine for 12 weeks.Then their MMSE and ADL were evaluated and the Vm and PI were measured by TCD before and after treatment,and P300 was detected before and after treatment.The side effects of the drugs were recorded at the same time.RESULTS The scales of MMSE and ADL were improved after nimodipine treatment(P0.01),the Vm and PI were improve after nimodipine treatment(P0.05),P300 latencies reduced and amplitudes increased significantly after nimodipine treatment(P0.01),The side effects of nimodipine were mild.CONCLUSION Nimodipine has a safe and therapeutic effect on mild/medium Vascular dementia.
Nimodipine
Vascular dementia
Therapeutic effect
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AIM: To observe the effect of nimodipine on the severe brain injury. METHODS: Nimodipine was ccsed for acute severe brain injury patients early in 6 hours after wounded. The effect and safety were observed in an open trial. RESULTS: The mortality and morbidity of 20 patients decreased significantly by the use of nimodipine in comparisom with another 20 patients treated normally. CONCLUSION: Nimodipine is benefit to severe brain injury patients.
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Gerbil
Dizocilpine
Brain ischemia
Brain damage
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Objective:To evaluate the effect and safty of nimodipine(capsules) to treat cerebral hemorrahge. Methods:30 patients were divided into two groups: control and treated. Patients of the treating group were treated with nimodipine 30 mg, 3 times a day, per os. It lasted 21 days for a course of treatment. Patients of the control group were treated with drugs other than nimodipine. Results: The effect of the treating group was better than that of the control group. Conclusion:It is suggested that nimodipine is a drug of choice for treating acute cerebral hemorrhage.
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Prevent and treat the cerebral vasospasm after subarachnoid hemorrhage with low dosage of Nimodipine
Objective:To study the therapeutic effect of low dosage of Nimodipine on the cerebral vasospasm(CVS) after subarachnoid hemorrhage (SAH).Method:39 cases by using Nimodipine and 21 cases in control group.The patients in Nimodipine group were transfused 4～10mg Nimodipine per day for 2～3 weeks.After that were changed to oral with 20～40mg 3/d for another 1-2 weeks(total 4 weeks).The control group was only treated in regular way for 4 weeks.Results:The incident and lethality rates of CVS after SAH in Nimodipine group were significantly lower than those in SAH control group (P0.05 and P0.001).Conclusion:low dosage of Nimodipine has significant therapeutic effect to prevent and treat cerebral vasospasm after SAH.
Nimodipine
Cerebral Vasospasm
Therapeutic effect
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Objective:To compare the curative effects between fluarizine and nimodipine in treating migraine. Methods:101 patients with migraine were randomly divide into two groups and were treated with fluarizine (group fluarizine, 51 cases) and nimodipine (group nimodipine, 50 cases), and evaluate the headache. A comparison between the times needed for controlling symptom after administration of the two drugs was made. Results:The effective rate by using fluarizine was 82.4% and that by nimodipine was 80%. In the controlled cases, the headache controlling rate was 40.5% after two weeks of administration of fluarizine, higher than that of nimodipine, which was only 15%. Conclusion:Fluarizine is an effective drug for migraine. It can relieve the symptom quickly and reduce economic burden of the patients.
Nimodipine
Drug Administration
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The effects of nimodipine on symptomatic cerebral vasospasm after subarachnoid hemorrhage in rabbits
Objective To study the effects of nimodipine on symptomatic cerebral vasospasm after subarachnoid hemorrhage(SAH)in rabbits.Methods The experimental symptomatic cerebral vasospasm was induced.Nimodipine was given intravenously in SAH+Nimodipine group.The neurological deficits,hemorrheologic changes and transmission electron microscopic examinations were observed and compared.Results By applying nimodipine,the neurological deficits were gradually improved and the hemorrheologic changes showed significant improvements.Meanwhile it was tested by transmission electron microscopic that pathological changes of SAH group were severer than that of SAH+Nimodipine group.Conclusions Nimodipine given early after SAH may show effects on symptomatic cerebral vasospasm in rabbits remarkably.
Nimodipine
Cerebral Vasospasm
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Objective To observe the effect of Nimodipine injection on DCVS after SAH.Methods 60 cases of SAH were divided into 2 groups randomly:Nimodipine group and control group.Both groups were given routine treatment.Nimodipine group was transfused with Nimodipine continuously.Results The incidence of DCVS and mortality in Nimodipine group were significantly lower than those in control group.Conclusion Nimodipine injection has a good effect on the prevention of DCVS after SAH.
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Clinical effect of nimodipine on postoperational patients with hypertensive intracerebral hemorrhage
Objective: To observe the effect of nimodipine on postoperational patients with hypertensive intracerebral hemorrhage. Methods: 60 of patients were divided into group of control and group of nimodipine treatment, all patients were observed by clinical curative effect.Nimodipine was performed with nimodipine group within 6h after operation and last 14d. Assessment of clinical curative effect were used by blind analysis. Results: After treatment, there were mild and moderate disability in 18 cases, severe disability in 6 cases, vegetative state in 2 and death in 3 cases in nimodipine treatment group. Good recover rate was 83.33% in nimodipine treatment group. The clinical curative effect in treatment group were significantly better than in the control group. Conclusion: Nimodipine is safe and effective for preventing the postoperational patients with hypertensive intracerebral hemorrhage from brain damage,reducing the mortality and improving the survival rate and life quality.
Nimodipine
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