中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2006年
3期
185-187
,共3页
背景:脑梗死多与血瘀证密切相关,血液流变学异常改变常表现为血黏度和红细胞压积增高.等容血液稀释疗法通过放血并移走一定量的红细胞,同时补充等容量的稀释剂,可降低全血黏度.目的:观察补气中药黄芪注射液和等容血液稀释疗法对脑梗死血瘀证患者血液流变学的改善作用.设计:随机对照实验,病例-对照分析.对象:脑梗死组为2002-03/2004-03华中科技大学附属协和医院收治的老年缺血性脑血管病住院患者64例,所有患者年龄>60岁,同时符合血瘀证诊断标准,按随机数字表法分为常规治疗组和中西医治疗组两组各32例.以正常体检的47名年龄相似的健康人为正常对照组.单位:华中科技大学同济医学院附属协和医院.方法:常规治疗组采用脑梗死常规方法治疗,包括扩容、降黏、抗凝、阻滞血小板凝聚、脱水及一般对症支持治疗.中西医治疗组在常规对症治疗基础上加用等容血液稀释和益气中药黄芪注射液治疗:从患者静脉抽取总血量的10%(450～650 mL),继之静脉注射等量胶体液,每隔5 d治疗1次,连续治疗3次;黄芪注射液50 mL加入生理盐水250 mL静脉滴注,1次/d,连用3周.主要观察指标:①常规治疗组和中西医治疗组治疗前后血液流变学各指标比较.②脑梗死组和正常对照组血液流变学各指标比较.结果:按意向处理分析,64例患者和47名正常人均进入结果分析.①脑梗死组和正常对照组比较:脑梗死组全血比黏度、红细胞压积和纤维蛋白原高于正常对照组[(3.90±0.73),(3.40±0.28)mpa·s;(46.39±6.03)%,(42.61±2.91)%;(3.25±0.75),(3.08±0.46)g/L,P<0.01,0.05],红细胞变形指数低于正常对照组(0.958±0.006,0.961±0.004,P<0.05)②常规治疗组和中西医治疗组比较:治疗前无差异,治疗后中西医治疗组全血黏度、红细胞压积和纤维蛋白原均低于常规治疗组[(3.90±0.52),(4.21±0.68)mpa·s;(43.80±3.29)%,(48.47±4.50)%;(3.31±0.60),(3.68±0.67)g/L,P<0.01,0.05].结论:对血瘀证的老年脑梗死患者用等容血液稀释疗法加益气中药黄芪注射液治疗,有较好的降低血黏度、改善血液流变学、减轻症状的作用.
揹景:腦梗死多與血瘀證密切相關,血液流變學異常改變常錶現為血黏度和紅細胞壓積增高.等容血液稀釋療法通過放血併移走一定量的紅細胞,同時補充等容量的稀釋劑,可降低全血黏度.目的:觀察補氣中藥黃芪註射液和等容血液稀釋療法對腦梗死血瘀證患者血液流變學的改善作用.設計:隨機對照實驗,病例-對照分析.對象:腦梗死組為2002-03/2004-03華中科技大學附屬協和醫院收治的老年缺血性腦血管病住院患者64例,所有患者年齡>60歲,同時符閤血瘀證診斷標準,按隨機數字錶法分為常規治療組和中西醫治療組兩組各32例.以正常體檢的47名年齡相似的健康人為正常對照組.單位:華中科技大學同濟醫學院附屬協和醫院.方法:常規治療組採用腦梗死常規方法治療,包括擴容、降黏、抗凝、阻滯血小闆凝聚、脫水及一般對癥支持治療.中西醫治療組在常規對癥治療基礎上加用等容血液稀釋和益氣中藥黃芪註射液治療:從患者靜脈抽取總血量的10%(450～650 mL),繼之靜脈註射等量膠體液,每隔5 d治療1次,連續治療3次;黃芪註射液50 mL加入生理鹽水250 mL靜脈滴註,1次/d,連用3週.主要觀察指標:①常規治療組和中西醫治療組治療前後血液流變學各指標比較.②腦梗死組和正常對照組血液流變學各指標比較.結果:按意嚮處理分析,64例患者和47名正常人均進入結果分析.①腦梗死組和正常對照組比較:腦梗死組全血比黏度、紅細胞壓積和纖維蛋白原高于正常對照組[(3.90±0.73),(3.40±0.28)mpa·s;(46.39±6.03)%,(42.61±2.91)%;(3.25±0.75),(3.08±0.46)g/L,P<0.01,0.05],紅細胞變形指數低于正常對照組(0.958±0.006,0.961±0.004,P<0.05)②常規治療組和中西醫治療組比較:治療前無差異,治療後中西醫治療組全血黏度、紅細胞壓積和纖維蛋白原均低于常規治療組[(3.90±0.52),(4.21±0.68)mpa·s;(43.80±3.29)%,(48.47±4.50)%;(3.31±0.60),(3.68±0.67)g/L,P<0.01,0.05].結論:對血瘀證的老年腦梗死患者用等容血液稀釋療法加益氣中藥黃芪註射液治療,有較好的降低血黏度、改善血液流變學、減輕癥狀的作用.
배경:뇌경사다여혈어증밀절상관,혈액류변학이상개변상표현위혈점도화홍세포압적증고.등용혈액희석요법통과방혈병이주일정량적홍세포,동시보충등용량적희석제,가강저전혈점도.목적:관찰보기중약황기주사액화등용혈액희석요법대뇌경사혈어증환자혈액류변학적개선작용.설계:수궤대조실험,병례-대조분석.대상:뇌경사조위2002-03/2004-03화중과기대학부속협화의원수치적노년결혈성뇌혈관병주원환자64례,소유환자년령>60세,동시부합혈어증진단표준,안수궤수자표법분위상규치료조화중서의치료조량조각32례.이정상체검적47명년령상사적건강인위정상대조조.단위:화중과기대학동제의학원부속협화의원.방법:상규치료조채용뇌경사상규방법치료,포괄확용、강점、항응、조체혈소판응취、탈수급일반대증지지치료.중서의치료조재상규대증치료기출상가용등용혈액희석화익기중약황기주사액치료:종환자정맥추취총혈량적10%(450～650 mL),계지정맥주사등량효체액,매격5 d치료1차,련속치료3차;황기주사액50 mL가입생리염수250 mL정맥적주,1차/d,련용3주.주요관찰지표:①상규치료조화중서의치료조치료전후혈액류변학각지표비교.②뇌경사조화정상대조조혈액류변학각지표비교.결과:안의향처리분석,64례환자화47명정상인균진입결과분석.①뇌경사조화정상대조조비교:뇌경사조전혈비점도、홍세포압적화섬유단백원고우정상대조조[(3.90±0.73),(3.40±0.28)mpa·s;(46.39±6.03)%,(42.61±2.91)%;(3.25±0.75),(3.08±0.46)g/L,P<0.01,0.05],홍세포변형지수저우정상대조조(0.958±0.006,0.961±0.004,P<0.05)②상규치료조화중서의치료조비교:치료전무차이,치료후중서의치료조전혈점도、홍세포압적화섬유단백원균저우상규치료조[(3.90±0.52),(4.21±0.68)mpa·s;(43.80±3.29)%,(48.47±4.50)%;(3.31±0.60),(3.68±0.67)g/L,P<0.01,0.05].결론:대혈어증적노년뇌경사환자용등용혈액희석요법가익기중약황기주사액치료,유교호적강저혈점도、개선혈액류변학、감경증상적작용.
AbstractBACKGROUND: Fas and P53 are important regulator and control gene which can promote apoptosis. They belong to the receptor family part of tumor necrotic factor/nerve growth factor. Their expression products have effects on apoptosis signal transmission, and can regulate and control cell apoptosis in cerebral ischemia-reperfusion injury. And puerarin can alleviate the level of cell apoptosis.OBJECTIVE: To observe the effect of puerarin on Fas and P53, the apoptosis-related gene of nerve cell in hippocampns CA1 region of rats af ter cerebral resuscitation.DESIGN: Randomized controlled trial. SETTING: Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: The experiment was carried out at Emergency Department, Tongji Hospital, Tongji Medical College, Huazhong University ofScience and Technology from September 2001 to Februray 2002. Totally 45 of 3 months old Wistar rats of clean grade were selected, and randomly divided into 3 groups: sham operation group, model control group and puerarin treatment group with 15 rats in each group.METHODS: Acute global brain ischemia-reperfusion models were established in rats of puerarin treatment group and model control group. In rats of sham operation group, stigmata of both flanks of the first cervical vertebrae were isolated, but bilateral vertebral arteries were not electric coagulated, and biolateral common carotid arteries were only isolatedwithout clamping close. Rats in puerarin treatment group were given puerarin injection 100 mg/kg, 1 hour before ischemia, and model control group were given normal saline in equivalence while rats in sham operation group were not given medicine. Death of rats in each group was performed separately in the 3rd, 6th, 12th, 24th and 48th hours after cerebral ischemia-reperfusion with 3 rats per group in each time. Hippocampus tissues of rats were isolated, and tissue slices were preparated. And the changes of- the protein expression levels and the number of apoptosis cells of rats in each group at different time point after cerebral ischemia-reperfusion were detected in immuno-histochemical method and end labelling in situ method. MAIN OUTCOME MEASURES: ① The number of positive cells inprotein expression of Fas and P53 in hippocampus CA1 region of rats in each group at different time point after cerebral ischemia-reperfusion was studied. ② Comparison of the number of apoptosis cells in hippocampus CA1 region of rats between groups at different time point after cerebral ischemia-reperfusion were studied, too.RESULTS: All the 45 rats enrolled in research were entered the stage of result analysis: ① The number of positive cells in protein expression of Fas in hippocampus CA1 region of rats in each group at different time point after cerebral ischemia-reperfusion: Obvious gene expression of Fas was not found in sham operation group. In contrast with model control group, obvious decrease was found at all time points after cerebral ischemi a-reperfusion in puerarin treatment group, and in the 6th, 12th, 24th and 48th hour the differences were significant [(15.0±4.3), (13.5±4.9); (40.7±3.4), (27.2±3.1); (37.0±4.8), (22.0±2.1); (24.7±4.1), (18.9±5.3)/mm; P < 0.05,P < 0.01]. ② The number of positive cells in protein expression of P53 in hippocanpus CA1 region of rats in each group at different time point after cerebral ischemia-reperfusion: Obvious gene expression of P53 was not found in sham operation group. In contrast with model control group, obvious decrease was found in the 24th and 48th hour after cerebral ischemiareperfusion in puerarin treatment group [(25.3±4.4), (12.8±2.7); (24.3±3.6), (10.9±3.0)/mm; P < 0.01]. ③ Comparison of the number of apoptosis cells in hippocampus CA1 region of rats between groups at different time point after cerebral ischemia-reperfusion :In contrast with model control group,obvious decrease was found in the 12th, 24th and 48th hour after cerebral is chemia-reperfusion in puerarin treatment group [(34.0±3.7), (21.0±3.7); (41.0±4.2), (33.0±4.8); (71.0±5.5), (41.0±3.4)/mm; P < 0.01].CONCLUSION: In rats which were given puerarin treatment, the expression of Fas decrease obviously in 6 to 48 hours after cerebral ischemiareperfusion, and the expression of P53 decreased obviously in the 24th to 48th hour after cerebral ischemia-reperfusion, and a descent tendency could be found in the number of apoptosis cells. These can further prove the cerebral protective effect of puerarin, and indicate that the inhibition of puerarin to cell apotosis after cerebral resuscitation is related to its effect on the decrease in protein expression of apoptosis-promoting gene, Fas and P53.Puerarin has a protective effect on cerebral ischemia-reperfusion injury of rats. In comparison with model control group, the expression of Fas in puerarin treatment group has an obvious decrease inthe 6th to 48th hour after cerebral ischemia-reperfusion, the expression of P53 has an obvious decrease in the 24th to 48th hour after cerebral ischemia-reperfusion, and the number of apoptosis cells decrease obviously, too, which further improves the cerebral protective effect of puerarin and indicates that the inhibition of puerarin to cell apoptosis after cerebral resuscitation is related to its effect on the decrease in protein expression of apoptosis-promoting gene Fas and P53.
