中华老年心脑血管病杂志
中華老年心腦血管病雜誌
중화노년심뇌혈관병잡지
Chinese Journal of Geriatric Heart Brain and Vessel Diseases
2015年
9期
960-963
,共4页
马晓娟%郭春雨%张莹%王琳%殷慧军%史大卓
馬曉娟%郭春雨%張瑩%王琳%慇慧軍%史大卓
마효연%곽춘우%장형%왕림%은혜군%사대탁
心肌梗死%活血祛瘀%肌钙蛋白I%内皮缩血管肽1%美托洛尔%中药配伍
心肌梗死%活血祛瘀%肌鈣蛋白I%內皮縮血管肽1%美託洛爾%中藥配伍
심기경사%활혈거어%기개단백I%내피축혈관태1%미탁락이%중약배오
myocardial infarction%BLOOD ACT STASIS REMOV%troponin I%endothelin-1%meto-prolol%COMPATIBILITY(TCD)
目的:观察活血及活血解毒配伍对急性心肌梗死大鼠心肌损伤的保护作用。方法选择雄性SD大鼠100只,随机分为:假手术组(等量生理盐水)、模型组(等量生理盐水)、活血组[芎芍胶囊0.39 g/(kg · d )]、活血解毒组[芎芍胶囊0.39 g/(kg · d)+黄连胶囊0.135 g/(kg · d)]、美托洛尔组[美托洛尔2.25 mg/(kg · d)],每组20只。造模24 h处死大鼠,观察心肌组织病理改变,T TC法测量心肌梗死面积,ELISA 法检测血清肌酸激酶同工酶(CK‐MB)、肌钙蛋白I(cTnI)、内皮素1、血管性假血友病因子(vWF)、血栓调节蛋白(TM )等指标。结果与假手术组比较,模型组心肌梗死面积、CK‐MB、cTnI、内皮素1、vWF、TM 明显升高(P<0.01)。与美托洛尔组比较,活血解毒组cTnI明显降低[(11.88±1.98)pg/ml vs (14.13±2.02)pg/ml],内皮素1、vWF明显降低(P<0.05,P<0.01)。与活血组比较,活血解毒组cTnI、内皮素1、vWF、TM 明显改善(P<0.05,P<0.01)。结论活血解毒配伍对心肌损伤发挥了较好的保护作用,显著优于单纯的活血化瘀。
目的:觀察活血及活血解毒配伍對急性心肌梗死大鼠心肌損傷的保護作用。方法選擇雄性SD大鼠100隻,隨機分為:假手術組(等量生理鹽水)、模型組(等量生理鹽水)、活血組[芎芍膠囊0.39 g/(kg · d )]、活血解毒組[芎芍膠囊0.39 g/(kg · d)+黃連膠囊0.135 g/(kg · d)]、美託洛爾組[美託洛爾2.25 mg/(kg · d)],每組20隻。造模24 h處死大鼠,觀察心肌組織病理改變,T TC法測量心肌梗死麵積,ELISA 法檢測血清肌痠激酶同工酶(CK‐MB)、肌鈣蛋白I(cTnI)、內皮素1、血管性假血友病因子(vWF)、血栓調節蛋白(TM )等指標。結果與假手術組比較,模型組心肌梗死麵積、CK‐MB、cTnI、內皮素1、vWF、TM 明顯升高(P<0.01)。與美託洛爾組比較,活血解毒組cTnI明顯降低[(11.88±1.98)pg/ml vs (14.13±2.02)pg/ml],內皮素1、vWF明顯降低(P<0.05,P<0.01)。與活血組比較,活血解毒組cTnI、內皮素1、vWF、TM 明顯改善(P<0.05,P<0.01)。結論活血解毒配伍對心肌損傷髮揮瞭較好的保護作用,顯著優于單純的活血化瘀。
목적:관찰활혈급활혈해독배오대급성심기경사대서심기손상적보호작용。방법선택웅성SD대서100지,수궤분위:가수술조(등량생리염수)、모형조(등량생리염수)、활혈조[궁작효낭0.39 g/(kg · d )]、활혈해독조[궁작효낭0.39 g/(kg · d)+황련효낭0.135 g/(kg · d)]、미탁락이조[미탁락이2.25 mg/(kg · d)],매조20지。조모24 h처사대서,관찰심기조직병리개변,T TC법측량심기경사면적,ELISA 법검측혈청기산격매동공매(CK‐MB)、기개단백I(cTnI)、내피소1、혈관성가혈우병인자(vWF)、혈전조절단백(TM )등지표。결과여가수술조비교,모형조심기경사면적、CK‐MB、cTnI、내피소1、vWF、TM 명현승고(P<0.01)。여미탁락이조비교,활혈해독조cTnI명현강저[(11.88±1.98)pg/ml vs (14.13±2.02)pg/ml],내피소1、vWF명현강저(P<0.05,P<0.01)。여활혈조비교,활혈해독조cTnI、내피소1、vWF、TM 명현개선(P<0.05,P<0.01)。결론활혈해독배오대심기손상발휘료교호적보호작용,현저우우단순적활혈화어。
Objective To study the role of promoting blood circulation and its combination with de‐toxication in protecting AMI rats against myocardial injury .Methods One hundred male SD rats were randomly divided into sham operation group ,model group ,promoting blood circulation group ,promoting blood circulation and detoxication group ,and metoprolol treatment group (20 in each group) .The animals were sacrificed 24 h after a model of AMI was established .Their myo‐cardial tissue lesions were observed by optical microscopy ,their myocardial infarction size was measured by TIC ,their serum levels of CK‐MB ,cTnI ,ET‐1 ,vWF ,and TM were measured by ELISA .Results The myocardial infarction size was significantly larger and the serum levels of CK‐MB ,cTnI ,ET‐1 ,vWF ,and TM were significantly higher in model group than in sham opera‐tion group (P<0 .01) .The serum levels of cTnI ,ET‐1 and vWF were significantly lower in pro‐moting blood circulation and detoxication group than in metoprolol treatment group ( P<0 .05 , P<0 .01) .The serum levels of cTnI ,ET‐1 ,vWF ,and TM were improved more signficantly in promoting blood circulation and detoxication group than in promoting blood circulation group (P<0 .05 ,P< 0 .01) .Conclusion Combined promoting blood circulation and detoxication can protect AMI rats against myocardial injury ,and its effect is significantly better than that of simple promoting blood circulation to remove blood stasis .