本文選題：丁苯酞 + 急性腦梗塞��； 參考：《河北醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:人類死亡的誘發(fā)因素中,腦血管病位居前2位。相較于西方國(guó)家,國(guó)內(nèi)腦血管病的患病人數(shù)以及死亡人數(shù)均要比心血管病多出很多。缺血性腦血管病,患病率相對(duì)偏高,并能夠誘發(fā)神經(jīng)元受損。缺血形成階段中,神經(jīng)元受損需經(jīng)歷多個(gè)環(huán)節(jié)和步驟,如自由基受損、谷氨酸的釋放及其毒性作用、細(xì)胞中的鈣含量增多以及炎癥級(jí)聯(lián)作用等。這些年,我們將自由基氧化、炎癥級(jí)聯(lián)兩種反應(yīng)及其誘發(fā)的繼發(fā)性腦損傷,納入研究行列。國(guó)內(nèi)外研究發(fā)現(xiàn)丁苯酞可以對(duì)不同的病理環(huán)節(jié)起作用,從而被視作治療急性缺血性腦卒中的一類新藥物。缺血性卒中演變進(jìn)程中,丁苯酞可以抑制和緩解腦組織損傷,使腦組織恢復(fù)正�；蚪咏５墓┭獱顟B(tài)。動(dòng)物實(shí)驗(yàn)早已證實(shí):丁苯酞可明顯縮小急性腦梗死大鼠腦細(xì)胞死亡的實(shí)際面積,緩解腦水腫,調(diào)節(jié)腦細(xì)胞異常的能量代謝,促進(jìn)側(cè)枝循環(huán)和正常的血流量;對(duì)神經(jīng)細(xì)胞的快速凋亡起抑制作用,同時(shí)也可以對(duì)抗血栓形成,避免血小板大量地聚集。但是對(duì)腦梗死后的炎癥反應(yīng)影響報(bào)道不多。本研究旨在對(duì)急性腦缺血病例給予丁苯酞,觀察用藥前后白介素6(IL-6)以及超敏CRP兩項(xiàng)指標(biāo)的變化,探討神經(jīng)功能缺損程度和IL-6之間的關(guān)系,為丁苯酞治療急性腦梗塞的機(jī)制提供更多地理論依據(jù)。方法:選擇發(fā)病時(shí)間48h的急性腦梗死病例共60例。對(duì)所有病例進(jìn)行隨機(jī)分組,一組為治療組(30例),另一組為對(duì)照組(30例);另選擇20名正常體檢者,設(shè)為正常組。急性腦梗死對(duì)照組病例接受常規(guī)療法,如阿司匹林、他汀類穩(wěn)定斑塊,輔助降壓以及降血糖及對(duì)癥等多種治療措施。治療組:以對(duì)照組用藥基礎(chǔ)上,加用丁苯酞氯化鈉注射液,劑量為100m1/次,靜脈滴注,2次/日;滴注時(shí)間50-70min;兩次靜滴時(shí)間間隔6h,對(duì)丁苯酞注射液進(jìn)行輸注時(shí),需選擇非PVC輸液器。全部病例的療程為14d;14天后給予口服丁苯酞軟膠囊,200mg/次,3次/日,持續(xù)30d.兩組患者均于住院當(dāng)天(第1d),治療后第7,14以及30d四個(gè)時(shí)段,參照美國(guó)衛(wèi)生研究院卒中量表(The national institutes of health stroke scale NIHSS)以及自理能力Barthel指數(shù)(BI)對(duì)兩組病例進(jìn)行評(píng)分。同時(shí),對(duì)兩組病例治療前后不同時(shí)段的超敏CRP和IL-6水平分別進(jìn)行檢測(cè),分析神經(jīng)功能缺損嚴(yán)重性和超敏CRP以及IL-6指標(biāo)存在的關(guān)聯(lián)。結(jié)果:1神經(jīng)功能損傷程度評(píng)分,在治療前,治療組和對(duì)照組無明顯差異;治療后,兩組的評(píng)分均較治療前有明顯改善,且其中治療組治療后的評(píng)分較前改善更為顯著(P0.05)。2超敏CRP和IL-6水平:治療組和對(duì)照組病例的超敏CRP和IL-6水平均顯著高于正常組,有統(tǒng)計(jì)學(xué)差異(P0.05);治療第7、14、30d,治療組和對(duì)照組患者血清超敏CRP和IL-6水平均低于治療前,且治療組病例的超敏CRP和IL-6檢測(cè)值的降低程度要高于對(duì)照組,有統(tǒng)計(jì)學(xué)差異(P0.05)。3針對(duì)急性腦梗死病例,NIHSS、BI評(píng)分和sCRP以及IL-6水平之間呈顯著正相關(guān)(P0.05)。結(jié)論:1急性腦梗死患者NIHSS、BI評(píng)分和sCRP以及IL-6水平之間呈顯著正相關(guān);2給予丁苯酞能顯著改善急性腦梗死患者神經(jīng)功能缺損程度;3下調(diào)sCRP、IL-6水平可能是丁苯酞發(fā)揮神經(jīng)保護(hù)作用的機(jī)制之一。
[Abstract]:Objective: of the leading factors of human death, cerebrovascular disease is the top 2. Compared with the western countries, the number of patients with cerebrovascular disease and the number of deaths are much more than cardiovascular disease. Ischemic cerebrovascular disease, the incidence of disease is relatively high, and can induce neuron damage. In the ischemic formation stage, neuron damage needs to experience a lot. Links and steps, such as free radical damage, the release of glutamic acid and its toxic effects, increased calcium content in cells and cascade of inflammation, we have included free radical oxidation, two reactions and induced secondary brain damage in these years. Domestic and foreign studies have found that butylphthalide can be used for different pathological links. It is considered as a new drug for the treatment of acute ischemic stroke. In the course of the evolution of ischemic stroke, butylphthalide can inhibit and alleviate brain tissue damage, make the brain restore normal or close to normal blood supply. Animal experiments have already proved that butylphthalide can significantly reduce the death of brain cells in rats with acute cerebral infarction The area, which alleviates brain edema, regulates the energy metabolism of abnormal brain cells, promotes the collateral circulation and normal blood flow, inhibits the rapid apoptosis of the nerve cells, and can also antagonize the formation of thrombus and avoid massive aggregation of platelets. However, there are few reports on the effect of the inflammatory reaction after cerebral infarction. This study aims at acute brain deficiency. The changes in the two indexes of interleukin 6 (IL-6) and hypersensitivity CRP were observed in the blood cases, and the relationship between the degree of nerve function defect and IL-6 was explored, and more theoretical basis was provided for the mechanism of butylphthalide in the treatment of acute cerebral infarction. Methods: 60 cases of acute cerebral infarction were selected at the time of the onset of 48h. The treatment group (30 cases), the other group was the control group (30 cases), and the other 20 normal subjects were selected as the normal group. The patients in the control group of acute cerebral infarction were treated with conventional therapy, such as aspirin, statin stable plaque, auxiliary antihypertensive and hypoglycemic and symptomatic treatment. The treatment group was based on the control group. With Butylphthalide and Sodium Chloride Injection, dosage of 100m1/, intravenous drip, 2 times / day, infusion time 50-70min and two time interval 6h, non PVC infusion apparatus should be selected when infusion of butylphthalide injection. The course of all cases is 14d; 14 days after 14 days, oral Butylphthalide Soft Capsules, 200mg/ times, and 3 / day, continuous 30D. two groups are all On the day of hospitalization (1D), at the four periods of 7,14 and 30d after treatment, the two groups were evaluated with reference to the apoplexy of the US Institutes of Health (The National Institutes of Health Stroke Scale NIHSS) and the self-care capacity Barthel index. The correlation between the severity of nerve function defect and the hypersensitivity CRP and the IL-6 index was analyzed. Results: there was no significant difference between the treatment group and the control group before the treatment. The score of the 1 nerve function damage degree was no significant difference before the treatment. The scores of the two groups were significantly improved after the treatment, and the scores of the treatment group were more significant than those before the treatment (P0.05). .2 hypersensitivity CRP and IL-6 level: the hypersensitivity CRP and IL-6 water in the treatment group and the control group were significantly higher than the normal group, with a statistically significant difference (P0.05). The serum hypersensitivity CRP and IL-6 water in the treatment group and the control group were lower than before the treatment, and the degree of hypersensitivity CRP and IL-6 detection in the treatment group was higher than that of the control group. There was a significant positive correlation between NIHSS, BI score and sCRP and IL-6 levels (P0.05) for acute cerebral infarction (P0.05). Conclusion: 1 there was a significant positive correlation between NIHSS, BI score and sCRP and IL-6 levels in patients with acute cerebral infarction; 2 the degree of neurological impairment in patients with acute cerebral infarction was significantly improved; 3 The level of sCRP and IL-6 may be one of the mechanisms of neuroprotective effect of butylphthalide.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R743.3

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本文編號(hào)：2034420