Effect of electroacupuncture at Neiguan(PC6)at different time points on myocardial ischemia reperfusion arrhythmia in rats

OBJECTIVE:To observe the effects of electroacupuncture at Neiguan(PC6)at different time points on reperfusion arrhythmia(RA)after myocardial ischemia and reperfusion in rats,and to investigate the correlation of this protective effect with nerve growth factor(NGF),tyrosine kinase A(Trk A),tyrosine hydroxylase(TH),and norepinephrine(NE).METHODS:A total of 72 Sprague-Dawley male rats were randomly divided into six groups(n=12 rats/group):normal group(Norm),sham operation group(Sham),ischemia reperfusion group(I/R),pre-ischemic electroacupuncture group(EAI),pre-reperfusion electroacupuncture group(EAII),post-reperfusion electroacupuncture group(EAIII).The myocardial ischemia-reperfusion injury(MIRI)model was induced by occlusion of left anterior descending coronary artery for 20 min followed by reperfusion for 40 min in rats.With no intervention in the Norm group and only threading without ligation in the Sham group.Electroacupuncture pretreatment at 20 min/d for 7 d before ligation in the EAⅠgroup,20 min of electroacupuncture before reperfusion in the EAII group and 20 min of electroacupuncture after reperfusion in the EAIII group.The electrocardiogram(ECG)of each group was recorded throughout the whole process,and the success of the MIRI model was determined based on the changs of J-point and T-wave in the ECG.The arrhythmia score was used to record premature ventricular contractions,ventricular tachycardia and ventricular fibrillation during the reperfusion period to assess the reperfusion induced arrhythmias.The expression levels of NGF,Trk A,TH protein were measured by Western blot.Moreover,the expression levels of plasma and myocardial NE levels were detected by enzyme linked immunosorbent assay.RESULTS:The differences between Norm group and Sham group were not statistically significant in all indexes.Arrhythmia score,myocardial NGF,Trk A,TH,and NE expression were significantly higher in the I/R group compared with the Sham group.Arrhythmia score,myocardial NGF,Trk A,TH,and NE expression were significantly lower in each EA group compared with the I/R group.CONCLUSION:Electroacupuncture at Neiguan(PC6)at different time points can reduce the incidence and severity of reperfusion arrhythmias in rats.This protective effect is related to electroacupuncture regulating NGF,Trk A,TH,NE expression and reducing sympathetic hyperactivation.

Effect of electroacupuncture pretreatment on adenine nucleotides in myocardial tissues of rats with myocardial ischemia-reperfusion injury detected by high performance liquid chromatography(HPLC)

Objective:To observe the effect of electroacupuncture(EA)pretreatment on adenine nucleotides in the myocardial tissues of the myocardial ischemia-reperfusion injury(MIRI)rats,and to explore the mechanism of EA pretreatment on myocardial prevention and protection in MIRI rats.Methods:Forty SPF male Sprague-Dawley(SD)rats were randomly divided into 5 groups:a blank group,a sham operation group,a model group,an EA at Neiguan(PC 6)group and an EA at Hegu(LI 4)group,with 8 rats in each group.Rats in the blank group only received binding to the rat plate,30 min/time,once a day for 7 d;on the 7th day,rats in the sham operation group were subjected to threading for 40 min at the left anterior descending coronary artery without ligation,and then the rats were allowed to stand for 60 min before collection of the specimens;on the 7th day,rats in the model group were subjected to threading at the left anterior descending coronary artery with ligation,for 40 min before the blood flow was restored,and then the rats were allowed to stand for 60 min before collection of the specimens;on the 7th day of pretreatment with EA at Neiguan(PC 6)or Hegu(LI 4)for 30 min per day(once a day for 7 d),rats in the EA at Neiguan(PC 6)group and EA at Hegu(LI 4)group were subjected to modeling and sample collection same as in the model group.The left ventricular myocardium of the lower left anterior descending coronary artery was collected from rats in all 5 groups.Hematoxylin-eosin(HE)staining and transmission electron microscope(TEM)were used to observe the changes in myocardial pathological morphology.The change in the adenine nucleotide level of myocardial tissue was measured by high performance liquid chromatography(HPLC).Results:The HE staining and ultrastructure showed that the myocardial injury was severer in the model group compared with the sham operation group.Compared with the model group,the myocardial injury in the EA at Neiguan(PC 6)and the EA at Hegu(LI 4)groups was mild or hardly any.The adenine nucleotide levels in the sham operation group and the model group were all decreased compared with the blank group(all P<0.05);compared with the sham operation group,the adenine nucleotide level of the model group was also decreased,but the difference was not statistically significant(P>0.05);compared with the model group,the adenine nucleotide level in the EA at Neiguan(PC 6)group was increased(P<0.05),and the adenine nucleotide level in the EA at Hegu(LI 4)group was significantly increased(P<0.01).The adenine nucleotide level in the EA at Hegu(LI 4)group was higher than that in the EA at Neiguan(PC 6)group,but the difference was not statistically significant(P>0.05).Compared with the EA at Neiguan(PC 6)group,the levels of adenosine triphosphate(ATP),adenosine diphosphate(ADP)and adenosine monophosphate(AMP)in the EA at Hegu(LI 4)group were significantly increased(all P<0.01).Conclusion:Both EA at Neiguan(PC 6)and Hegu(LI 4)can alleviate the pathological damage to myocardium in MIRI rats,and increase the adenine nucleotide level in myocardial tissues,and thus protect MIRI rats.EA at Hegu(LI 4)has a better protective effect than Neiguan(PC 6).

Electroacupuncture Pretreatment at Neiguan (PC 6) attenuates autophagy in rats with myocardial ischemia reperfusion through the phosphatidylinositol 3-kinase-Akt-mammalian target of rapamycin pathway

OBJECTIVE: To investigate the protective efficacy of electroacupuncture(EA) pretreatment at Neiguan(PC6) on myocardial ischemia-reperfusion(I/R) in rats.METHODS: Fifty rats were randomly divided into five groups(n = 10): sham operation group, model group(underwent in vivo myocardial I/R), EA pretreatment group [EA at Neiguan(PC 6) 1 week before I/R], wortmannin group(1 week before I/R, the PI3K inhibitor, wortmannin, was injected), EA pretreatment + wortmannin group(both pretreatments were performed simultaneously). After establishing the I/R model, 2,3,5-triphenyltetrazolium chloride(TTC) staining was used to analyze the weight and area of the myocardial infarction tissue.The biosignal and pressure test system was used to determine the left ventricular systolic mean pressure(LVSP), left ventricular end-diastolic pressure(LVEDP), fractional shortening(FS), and ejection fraction(EF). Ultraviolet spectrophotometry was used to determine the expression of creatine kinase(CK)-MB, inducible nitric oxide synthase(i NOS), and total antioxidant capacity(T-AOC) in the serum. The expression of autophagy-related protein 13(ATG13), mammalian target of rapamycin(m TOR), and phosphatidylinositol 3-kinase(PI3K) in cardiac muscle cells was determined by immunofluorescence. Hematoxylin and eosin staining was used to observe autophagy-related pathological changes in rat cardiomyocytes, and ultrastructural changes of cardiomyocytes were examined by transmission electron microscopy.RESULTS: In this study, the infarction size and tissue weight of the EA pretreatment group were decreased compared with the model group(P <0.0001). Furthermore, compared with the model group, the LVEDP values of the EA pretreatment group were significantly reduced(P = 0.0091), and the LVSP, FS, and EF values were slightly increased (P = 0.0007, 0.0020, 0.0031). EA pretreatment also significantly decreased the expression of CK-MB and i NOS, while it increased the expression of T-AOC in the serum of rats with I/R injury(P <0.0001). Furthermore, EA pretreatment slightly widened the myocardial fiber space, reduced necrosis and myocardial cell swelling and maintained the nucleus and mitochondria structure intact.CONCLUSION: EA pretreatment promoted autophagy flux and alleviated myocardial I/R injury through the PI3K-Akt-m TOR pathway.

通过JAK2/STAT3信号通路观察电针减轻MIRI炎性反应机制研究

目的通过观察电针“内关”穴观察心肌缺血再灌注损伤(MIRI)大鼠心肌组织中的酪氨酸激酶-2(JAK2)和信号转导及转录激活因子-3(STAT3)表达,探讨电针上调JAK2/STAT3信号通路,促进抗炎因子表达,减少MIRI损伤的作用机制。方法将超声心动图正常的30只雄性SD大鼠随机分为假手术组、模型组和电针组,每组10只。模型组和电针组采用冠状动脉左前降支(LAD)结扎法制备MIRI模型,假手术组仅穿线不结扎。电针组在造模术后第1、3、5天进行双侧“内关”穴电针(疏密波,2 Hz/100 Hz,2 mA)干预,每天1次,每次20 min。采用超声心动图观察术后第1、3、5天大鼠左心室射血分数(LVEF)以评估心功能;HE染色观察大鼠心肌病理形态变化;马松染色观察大鼠心肌纤维化情况;ELISA检测心肌组织中IL-4、IL-6的表达;免疫组化检测心肌组织中IL-1β、IL-10的表达情况;Western blot法测定梗死区心肌组织JAK2、p-JAK2、STAT3、p-STAT3蛋白表达。结果与假手术组比较,模型组大鼠术后EF明显降低(P<0.05),纤维化面积增大(P<0.05),IL-4、IL-6、IL-10、IL-1β含量均升高(P<0.05),JAK2、p-JAK2、STAT3、p-STAT3蛋白表达含量均升高(P<0.05);与模型组比较,电针组大鼠EF上升(P<0.05),电针组大鼠纤维化面积减小(P<0.05),IL-4、IL-10含量升高,IL-6、IL-1β含量下降(P<0.05),JAK2、p-JAK2、STAT3、p-STAT3蛋白表达含量均升高(P<0.05)。结论电针内关穴可显著上调JAK2/STAT3信号通路,减少促炎因子的分泌,增加抗炎因子的表达,减轻大鼠心肌缺血再灌注损伤。

电针预处理对心肌缺血再灌注损伤小鼠下丘脑腹内侧核神经元活动的影响

目的 观察电针预处理心经经穴对心肌缺血再灌注损伤(myocardial ischemia-reperfusion injury, MIRI)小鼠下丘脑腹内侧核(ventromedial hypothalamic nucleus, VMH)神经元活动的影响,探讨电针预处理抗MIRI的中枢调控机制。方法 将36只C57BL/6小鼠随机分为假手术组、模型组、电针组,每组12只;电针组选取双侧神门、通里穴进行电针预处理,每次30 min,每日1次,共干预7 d,末次电针预处理结束后1 h内进行MIRI模型复制;模型组和假手术组小鼠不予电针。采用Powerlab多导生理记录仪和Chart软件记录并分析各组小鼠模型复制前、缺血30 min、再灌注120 min时ST段电压值的变化;苏木精—伊红(hemaxylin eosin, HE)染色法观察各组小鼠心肌组织病理变化;免疫荧光染色法观察各组小鼠VMH中c-fos表达情况以及模型组小鼠VMH中c-fos分别与谷氨酸、γ-氨基丁酸共表达情况;采集、分析和比较各组小鼠VMH神经元电活动。结果 与假手术组比较,模型组小鼠结扎30 min及再灌注120 min时ST段电压值均显著升高(P<0.05),HE染色可见小鼠心肌组织损伤严重,VMH中c-fos阳性细胞数显著增加(P<0.05),VMH锥体神经元放电次数显著增加(P<0.05),中间神经元放电次数显著减少(P<0.05),VMH神经元局部场电位频谱能量增强,放电频率较为密集;与模型组比较,电针组小鼠结扎30 min及再灌注120 min时ST段电压值均显著降低(P<0.05),HE染色可见心肌组织损伤较轻,VMH中c-fos阳性细胞数显著减少(P<0.05),VMH锥体神经元放电次数显著减少(P<0.05),中间神经元放电次数差异无统计学意义(P>0.05),VMH神经元局部场电位频谱能量降低,放电频率较为疏散。模型组小鼠VMH中c-fos与谷氨酸能神经元的共表达量高于与γ-氨基丁酸能神经元的共表达量(P<0.05)。结论 电针预处理心经经穴可降低小鼠VMH锥体神经元放电频率和c-fos表达水平,减轻心肌损伤,VMH中谷氨酸能神经元参与了电针抗MIRI的中枢整合机制。

电针“内关”对心肌缺血再灌注损伤内皮素及超微结构的影响

目的 :探讨“内关”在心肌缺血再灌注损伤过程中对心肌细胞的保护作用。方法 :电针家兔左右侧“内关”穴 2 0min后 ,结扎左冠状动脉前降支 ,心电图 (ECG)监测。 4 0min后恢复灌流 ,再灌注 1小时 ,取静脉血及心肌组织 ,观察血浆内皮素 (ET)及透射电镜下组织超微结构的变化。结果 :针刺“内关”组ET含量明显降低 (P <0 0 1) ,心肌组织损伤轻微 ,肌纤维正常走向 ,少量线粒体空泡变 ,肌丝无明显坏死、溶解。结论 :电针“内关”可明显降低缺血再灌注损伤的程度 。

电针预处理对兔脊髓缺血再灌注损伤细胞内Ca^(2+)变化的影响

目的 :探讨重复电针预处理诱导缺血耐受对脊髓缺血再灌注损伤保护作用的机制。方法 :76只雄性新西兰大白兔随机分成 4组 :对照组 (C组 ) ,戊巴比妥钠组 (SP组 ) ,假手术组 (S组 ) ,电针预处理组 (EA组 )。最后一次预处理后 2 4h ,阻闭肾下腹主动脉 ,制作兔脊髓缺血模型 ;S组动物手术操作同C组 ,但不阻闭腹主动脉。分别于阻闭后不同时相点测定细胞内Ca2 + 含量 ,并分别对动物后肢运动功能评分。结果 :EA组脊髓组织细胞内Ca2 + 含量显著低于C组和SP组各时相值 (P <0 0 1) ,神经功能评分EA组明显高于C组 (P <0 0 1) ,C组和SP组细胞内Ca2 + 和神经功能评分无显著性差异 (P >0 0 5 )。结论 :电针预处理具有降低脊髓组织细胞内Ca2 + 含量 ,防止Ca2 + 超载 ,稳定细胞内环境的能力 ,对腹主动脉阻断所致的脊髓缺血再灌注损伤具有良好的保护作用。

电针及天麻对大鼠脑缺血再灌注后神经细胞凋亡及相关蛋白Bcl-2、Bax表达的影响

目的 :探讨电针及天麻对缺血性脑损伤的神经保护机制。方法 :采用大鼠大脑中动脉闭塞模型造成脑局灶性缺血 2h ,再灌注 2 4h。以HE染色 ,TUNEL标记和免疫组化的方法观察使用电针及天麻后神经细胞凋亡及相关蛋白表达的变化。结果 :针药结合组显示神经元形态病理改变明显减轻 ,残存细胞率增加更明显 ,显著降低残存细胞中TUNEL阳性细胞的百分率。Bcl 2 /Bax的表达比例增加更显著。结论 :电针、天麻及二者结合有抗脑缺血再灌注后神经细胞凋亡的作用 。

针刺手厥阴心包经穴对心肌缺血再灌注损伤细胞凋亡的影响

目的 :探讨针刺手厥阴经穴治疗心血管疾病的机理。方法 :电针大鼠心包经穴位 2 0min后 ,结扎左冠状动脉前降支 40min ,心电图 (ECG)监测 ,再电针穴位 2 0min ,松扎 ,恢复灌流 60min,摘取心脏 ,制成细胞悬液 ,流式细胞仪检测。结果 :模型组出现典型的细胞凋亡峰 ,凋亡率明显升高 ,针刺心包经穴组的凋亡率有明显降低 ,与模型组比较差异均有非常显著性意义 (P <0 0 1 )。结论 :针刺手厥阴经穴能有效地抑制心肌细胞的凋亡 。

β-肾上腺素受体后信号转导通路介导电针预治疗抗缺血性心律失常的作用

目的:观察电针预治疗对心肌缺血/再灌注心律失常的影响,并探讨心脏β肾上腺素受体信号转导站点中cAMP和Gsα蛋白在其中的作用。方法:采用结扎和再灌注大鼠左冠状动脉前降支的方法建立实验型心肌缺血/再灌注(I/R)模型。40只雄性大鼠随机分为正常对照(NC)组、缺血再灌注(IR)组、缺血再灌注加电针(EA)组和缺血再灌注加电针加心得安(EAP)组。观察比较电针预治疗对再灌注10min内心律失常评分、缺血心肌cAMP含量和Gsα蛋白表达的影响。结果:与NC组比较,IR组于再灌注10min内心律失常评分明显升高(P<0·01);与IR组比较,EA组心律失常发生率明显降低(P<0·01),而EAP组心律失常评分与IR组相近,亦明显高于EA组(P<0·01)。各组大鼠缺血心肌cAMP含量和Gsα蛋白表达结果与心律失常评分结果相似。电针预治疗可以明显减低I/R性损伤引发的心律失常的发生率,抑制I/R后引起的缺血心肌cAMP含量和Gsα蛋白的异常升高,β-肾上腺素受体阻断剂心得安可以抑制其保护作用。结论:电针预治疗具有抗心律失常作用,β-肾上腺素受体信号转导站点中cAMP和Gsα蛋白参与了介导针刺预处理改善上述心肌缺血性损害的作用。

电针对胃缺血再灌注影响的激光血流成像方法研究

目的:观察电针对胃血流灌注的影响,寻找反映胃血流变化的研究方法。方法:在建立一种新的结扎大鼠胃右动脉而形成胃缺血再灌注模型的基础上,电针"足三里"穴,采用激光多普勒血流灌注成像仪(LDPI)对胃血流灌注图像予以显示,分析电针对胃血流灌注的作用。结果:①新的胃缺血再灌注模型显像清晰。电针组在缺血30 min内,缺血程度较对照组为轻;再灌注后血流的恢复效果也优于对照组。②在结扎25 min时,电针组血流量的变化均值为(-0.50±0.18)PU,与对照组(-0.90±0.16)PU比较,差异有显著性意义(P<0.05)。结论:电针可改善并促进缺血再灌注胃的血流供应;结扎和松解胃右动脉而形成的胃缺血和再灌注模型可以用于针灸研究中。

针刺手厥阴经穴对缺血再灌注损伤大鼠心肌钙泵活性及基因表达的影响

目的:观察针刺心包经“内关”“郄门”穴治疗心肌缺血的作用机制。方法:将大鼠随机分为5组,假手术组、缺血-再灌注模型组、针刺“内关”治疗组、针刺“郄门”治疗组、针刺“支沟”对照组。后3组电针相应穴位20min后,结扎冠状动脉左前降支40min,心电图(ECG)监测,再电针穴位20min,松扎,恢复灌流60min,摘取心脏,取心室肌制备心肌细胞肌浆网,定磷法测定三磷酸腺苷酶(Ca2+-ATPase)活性的高低;用Northen-Blot方法测定肌浆网Ca2+-ATPasemRNA的相对含量。结果:模型组Ca2+-ATPase活性明显降低,Ca2+-ATPasemRNA的表达下降。针刺心包经“内关”穴组和“郄门”穴组Ca2+-ATPase活性和Ca2+-ATPase mRNA表达均发生明显变化,与模型组比较均有非常显著性意义(P<0.01),针刺“支沟”穴组酶活性与基因的表达和模型组比较差异无显著性意义(P>0.05)。结论:针刺手厥阴心包经穴“内关”“郄门”穴可提高心肌细胞肌浆网Ca2+-ATPase的活性,促进Ca2+-ATPasemRNA基因的表达,减轻缺血再灌注损伤的程度,增强心肌的功能。

电针预治疗保护心肌缺血再灌注损伤——β-肾上腺素受体的耐受机制

目的:探讨电针预治疗对心肌缺血/再灌注性损伤的保护作用,以及心脏β-肾上腺素受体在其中扮演的角色。方法:采用结扎和再灌大鼠左冠状动脉前降支的方法建立实验性心肌缺血/再灌注(I/R)模型。40只雄性大鼠随机分为正常对照(NC)组、缺血再灌注(IR)组、缺血再灌注+电针(EA)组和缺血再灌注+电针+心得安(EAP)组。电针预处理方法是心肌缺血造模前连续3 d给予双侧“内关”穴电针,每次20 min,观察比较心肌缺血前反复电针预处理对心电图ST段、心肌缺血面积以及β1-肾上腺素受体蛋白表达的影响。结果:与NC组比较,IR组在缺血30 min及再灌注10 min后ST段明显抬高(均P<0.01);与IR组比较,EA组ST段抬高幅度明显降低(均P<0.01),而EAP组ST段抬高幅度与IR组相近,均明显高于EA组(P<0.01)。以梗塞区/危险区比值为指标的观察表明,IR组梗塞区/危险区比值明显高于NC组(P<0.01),而EA组该比值则明显低于IR组(P<0.01),EAP组该比值则与IR组相仿,明显高于EA组(P<0.01)。对β1-肾上腺素受体蛋白的观察表明,IR组该受体蛋白含量显著高于NC组(P<0.01),EA组与IR组相比,该蛋白含量则明显降低(P<0.01),而EAP组该蛋白含量却明显高于EA组(P<0.05),其值与IR组相近。结论:电针预治疗可以改善冠状动脉结扎引起的ST段抬高,减轻心肌缺血的程度,减少心肌梗塞面积,减低由于I/R导致β1-肾上腺素受体蛋白的过度表达,β-肾上腺素受体阻断剂心得安可以抑制其保护作用。可见,电针预治疗对心肌缺血具有保护作用,β-肾上腺素受体参与了介导针刺预处理改善上述心肌缺血性损害的作用。

电针内关对心肌缺血再灌注损伤的影响

目的 观察电针内关对心肌缺血再灌注损伤心肌肌酸激酶 (creatinekinase ,CK)和内源性保护物质腺苷的影响 ,探讨电针内关对心肌缺血再灌注损伤的保护作用及机制。方法 Wistar雄性大鼠 5 0只 ,随机分为假手术组、缺血再灌注模型组、电针内关组、电针列缺组和电针合谷组 ,结扎大鼠冠脉左前降支造成心肌缺血模型 ,检测心肌CK和腺苷 (adenosine ,Ado)含量。结果 内关穴组心肌CK含量低于模型组 (P <0 .0 5 ) ,内关组血清中Ado含量高于模型组 (P <0 .0 1 )。结论 电针内关穴减少心肌缺血再灌注损伤CK的释放 ,从而减轻心肌缺血再灌注损伤 ;促进内源性保护物质Ado的释放 ,从而在一定程度上对心肌缺血再灌注损伤心肌起到保护作用。

电针刺激对缺血再灌注心肌保护中IL-8的作用机制

目的 :观察电针刺激对缺血再灌注心肌保护中IL 8的作用机制。方法 :48例行冠脉搭桥术病人随机分为针刺组和对照组。于术前、体外循环转流前、停转流 60min和术毕取右心房血测定IL 8、SOD、MDA。转流前、停转流 60min取右心耳心肌组织 ,电镜观察心肌超微结构变化。结果 :两组IL 8含量持续上升 ,针刺组停转流 60min、术毕含量显著低于对照组。SOD、MDA于转流前至术毕呈现下降趋势 ,其中针刺组转流前SOD较对照组显著升高 ,而MDA显著降低。电镜观察显示停转流 60min针刺组心肌细胞损伤程度明显小于对照组。结论 :针刺能抑制IL 8的释放 ,减少氧自由基的产生 ,减轻受氧自由基的攻击程度 。

电针内关穴对心肌缺血再灌注损伤家兔心肌MDA、GSH-PX的影响

目的研究电针内关穴对心肌缺血再灌注损伤家兔心肌丙二醛、谷胱甘肽过氧化物酶含量的影响。方法将家兔随机分为4组:假手术组、模型组、电针内关组、电针列缺组。采用结扎左冠状动脉前降支30min,再灌注60min,建立心肌缺血再灌注损伤模型。应用分光光度法,观察电针对缺血再灌注损伤家兔心肌MDA、GSH-PX的影响。结果模型组家兔心肌MDA含量明显升高,而GSH-PX活性明显下降,与模型组、电针列缺组相比,电针内关组心肌MDA含量显著降低(P<0.05),而GSH-PX活性显著升高(P<0.01,P<0.05)。结论电针内关穴能显著降低缺血再灌注损伤心肌MDA含量,升高GSH-PX活性,达到抗缺血再灌注损伤的作用。

电针对心肌缺血再灌注损伤家兔心肌ICAM-1表达的影响

目的:研究电针对心肌缺血再灌注损伤家兔心肌细胞间黏附分子-1(ICAM-1)表达的影响。方法:将心电图正常的36只家兔随机分为4组:假手术组、模型组、电针内关组、电针列缺组。采用结扎左冠状动脉前降支30min,再灌注60min,建立心肌缺血再灌注损伤模型。应用免疫组织化学法,观察电针对缺血再灌注损伤家兔心肌ICAM-1表达的影响。结果:模型组家兔心肌ICAM-1表达明显升高,电针内关组心肌ICAM-1表达与模型组、电针列缺组比较显著降低(P<0.01)。结论:电针内关能显著降低缺血再灌注损伤心肌ICAM-1表达,从而减轻缺血再灌注后炎性病理损害,达到心肌保护作用。

电针对兔心肌缺血再灌注心律失常的影响

目的:观察电针"额旁1线"对家兔心肌缺血再灌注损伤所致的实验性心律失常的影响,并探讨其机制。方法:18只家兔随机分成3组,即假手术组(S组)、缺血再灌组(IR组)、电针治疗组(EA组)。采用结扎左冠状动脉前降支30min,再灌注60min后制备家兔心肌缺血再灌注模型,以再灌性心律失常、左心室功能和血清NO含量为观察指标。结果:EA组再灌注心律失常发生率低于IR组(P<0.05),左心室内压最大上升和下降速率及左室收缩压均高于IR组(P<0.01,P<0.05),血清NO含量显著提高(P<0.01)。结论:电针对心肌缺血再灌性心律失常具有保护作用,其机制可能与提高NO含量有关。

电针刺激和缺血预处理对猪心脏缺血再灌流损伤心肌功能的保护

目的 :观察电针刺激和缺血预处理对再灌注损伤心肌的保护作用。方法 :将 18头小型猪建立急性心肌缺血模型 ,随机分为 3组 ,对照组 (组Ⅰ )、缺血预处理组 (组Ⅱ )、针刺加缺血预处理组(组Ⅲ )。于缺血前 10min ,缺血 2 0min ,再灌注 2 0min、6 0min自左心耳采取标本 ,抽提组织总RNA ,对HSP70 mRNA进行定量 ,经静脉抽取血样本 ,测定CPK ,CK MB ,SOD ,MDA。超声多谱勒测定冠状动脉血流量 (CAF)。 结果 :①再灌注 2 0min和 6 0min时 ,组ⅠSOD值逐步降低 (P <0 0 5 ) ,组Ⅱ、组ⅢSOD值有升高趋势 ;组ⅠMDA值明显高于组Ⅱ、组Ⅲ。② 3组CPK ,CK MB均较对照值明显升高 (P <0 0 5 ,P <0 0 1) ,组Ⅰ的升高幅度明显大于组Ⅱ、组Ⅲ。③组ⅠHSP70 mR NA表达低于组Ⅱ和组Ⅲ。结论 :电针刺激可明显增强预适应拮抗心肌缺血再灌注造成的心肌损伤 。

电针对大鼠局灶脑缺血再灌注后脑内血管生长因子和血管抑制因子表达的影响

目的:探讨电针对缺血性脑卒中的作用机制。方法:线栓法制备Wistar大鼠局灶脑缺血再灌注模型。将大鼠随机分为正常组、模型组、电针组。选取双侧“合谷”穴为电针穴位,采用原位杂交法检测血管内皮生长因子(VEGF)mRNA的表达,免疫组化法检测血管生成素(Ang-1)和内皮抑素(Endostatin)蛋白的表达。结果:模型组VEGFmRNA、Ang-1蛋白、Endostatin蛋白的表达较正常组增加(P<0·05),电针组VEGFmRNA、Ang-1蛋白比模型组增加更明显(P<0·05),而En-dostatin蛋白表达增加较模型组明显下降,差异有显著性意义(P<0·05)。结论:电针可能通过上调血管生长因子和下调血管抑制因子的表达来促进局灶脑缺血再灌注后的血管新生。