临床心血管病杂志
臨床心血管病雜誌
림상심혈관병잡지
JOURNAL OF CLINICAL CARDIOLOGY
2010年
2期
112-115
,共4页
董红科%孙洪平%姚文明%张海锋%周艳丽%李新立
董紅科%孫洪平%姚文明%張海鋒%週豔麗%李新立
동홍과%손홍평%요문명%장해봉%주염려%리신립
心肌疾病%芪苈强心胶囊%美托洛尔%B型钠尿肽%肿瘤坏死因子-α
心肌疾病%芪藶彊心膠囊%美託洛爾%B型鈉尿肽%腫瘤壞死因子-α
심기질병%기력강심효낭%미탁락이%B형납뇨태%종류배사인자-α
cardiomyopathy%qiliqiangxin capsule%metoprolol%B-type natriuretic peptide%tumor necrosis factor-α
目的:初步探讨芪苈强心胶囊对阿霉素致心肌病大鼠心功能及血清因子的影响及其机制.方法:将29只SD大鼠中9只作为正常对照组,20只用作造模.造模大鼠2周内分6次腹腔注射阿霉素2.5 mg/kg作为心力衰竭(心衰)模型后,分为心衰组、芪苈强心组和美托洛尔组,后2组分别服用芪苈强心胶囊生粉(1 g/kg)和美托洛尔(10 mg/kg)治疗6周,正常对照组和心衰组以相同体积0.9%氯化钠溶液灌胃6周.超声心动图检测各组大鼠心功能指标,ELISA法检测大鼠血清肿瘤坏死因子-α(TNF-α)和B型钠尿肽(BNP)含量,心肌组织苏木素-伊红染色病理检验.结果:心衰组较正常对照组心功能显著降低,左心室收缩末期内径(LVESD)和左心室舒张末期内径(LVEDD)显著增加(P<0.01和P<0.05),左室射血分数(LVEF)和短轴缩短率(FS)显著降低(均P<0.01),血清BNP和TNF-α水平明显升高(均P<0.01).美托洛尔组较心衰组显著改善了大鼠的LVESD、 LVEDD、 LVEF和FS(均P<0.05),BNP显著低于心衰组(P<0.05).芪苈强心组较心衰组也改善了大鼠LVEF和FS(均P<0.05),显著降低心衰大鼠血清TNF-α水平(P<0.01).芪苈强心组与美托洛尔组心功能比较,差异无统计学意义(P>0.05),BNP和TNF-α均差异有统计学意义(P<0.05和P<0.01).病理切片经染色发现:心衰组心肌存在心肌部分坏死;美托洛尔组心肌纤维间有大量炎症细胞浸润,炎症周围的心肌纤维排列尚规则,横纹可见;芪苈强心组心肌纤维排列尚规则,横纹可见,心肌纤维间少量炎细胞浸润.结论:芪苈强心胶囊有改善心功能、降低血清炎性因子TNF-α水平及减轻心肌纤维炎症细胞浸润的作用.
目的:初步探討芪藶彊心膠囊對阿黴素緻心肌病大鼠心功能及血清因子的影響及其機製.方法:將29隻SD大鼠中9隻作為正常對照組,20隻用作造模.造模大鼠2週內分6次腹腔註射阿黴素2.5 mg/kg作為心力衰竭(心衰)模型後,分為心衰組、芪藶彊心組和美託洛爾組,後2組分彆服用芪藶彊心膠囊生粉(1 g/kg)和美託洛爾(10 mg/kg)治療6週,正常對照組和心衰組以相同體積0.9%氯化鈉溶液灌胃6週.超聲心動圖檢測各組大鼠心功能指標,ELISA法檢測大鼠血清腫瘤壞死因子-α(TNF-α)和B型鈉尿肽(BNP)含量,心肌組織囌木素-伊紅染色病理檢驗.結果:心衰組較正常對照組心功能顯著降低,左心室收縮末期內徑(LVESD)和左心室舒張末期內徑(LVEDD)顯著增加(P<0.01和P<0.05),左室射血分數(LVEF)和短軸縮短率(FS)顯著降低(均P<0.01),血清BNP和TNF-α水平明顯升高(均P<0.01).美託洛爾組較心衰組顯著改善瞭大鼠的LVESD、 LVEDD、 LVEF和FS(均P<0.05),BNP顯著低于心衰組(P<0.05).芪藶彊心組較心衰組也改善瞭大鼠LVEF和FS(均P<0.05),顯著降低心衰大鼠血清TNF-α水平(P<0.01).芪藶彊心組與美託洛爾組心功能比較,差異無統計學意義(P>0.05),BNP和TNF-α均差異有統計學意義(P<0.05和P<0.01).病理切片經染色髮現:心衰組心肌存在心肌部分壞死;美託洛爾組心肌纖維間有大量炎癥細胞浸潤,炎癥週圍的心肌纖維排列尚規則,橫紋可見;芪藶彊心組心肌纖維排列尚規則,橫紋可見,心肌纖維間少量炎細胞浸潤.結論:芪藶彊心膠囊有改善心功能、降低血清炎性因子TNF-α水平及減輕心肌纖維炎癥細胞浸潤的作用.
목적:초보탐토기력강심효낭대아매소치심기병대서심공능급혈청인자적영향급기궤제.방법:장29지SD대서중9지작위정상대조조,20지용작조모.조모대서2주내분6차복강주사아매소2.5 mg/kg작위심력쇠갈(심쇠)모형후,분위심쇠조、기력강심조화미탁락이조,후2조분별복용기력강심효낭생분(1 g/kg)화미탁락이(10 mg/kg)치료6주,정상대조조화심쇠조이상동체적0.9%록화납용액관위6주.초성심동도검측각조대서심공능지표,ELISA법검측대서혈청종류배사인자-α(TNF-α)화B형납뇨태(BNP)함량,심기조직소목소-이홍염색병리검험.결과:심쇠조교정상대조조심공능현저강저,좌심실수축말기내경(LVESD)화좌심실서장말기내경(LVEDD)현저증가(P<0.01화P<0.05),좌실사혈분수(LVEF)화단축축단솔(FS)현저강저(균P<0.01),혈청BNP화TNF-α수평명현승고(균P<0.01).미탁락이조교심쇠조현저개선료대서적LVESD、 LVEDD、 LVEF화FS(균P<0.05),BNP현저저우심쇠조(P<0.05).기력강심조교심쇠조야개선료대서LVEF화FS(균P<0.05),현저강저심쇠대서혈청TNF-α수평(P<0.01).기력강심조여미탁락이조심공능비교,차이무통계학의의(P>0.05),BNP화TNF-α균차이유통계학의의(P<0.05화P<0.01).병리절편경염색발현:심쇠조심기존재심기부분배사;미탁락이조심기섬유간유대량염증세포침윤,염증주위적심기섬유배렬상규칙,횡문가견;기력강심조심기섬유배렬상규칙,횡문가견,심기섬유간소량염세포침윤.결론:기력강심효낭유개선심공능、강저혈청염성인자TNF-α수평급감경심기섬유염증세포침윤적작용.
Objective:To investigate the effects of Qiliqiangxin capsule on heart function and serum factors in a rat model of cardiomyopathy induced by adriamycin.Method:The SD rats were randomly divided into two groups: normal control group and model building group. Rats in model building group were injected adriamycin (2.5 mg/kg) intravenously 6 times for 2 weeks. Rats surviving in model building group were randomly divided into three groups: heart failure group, Qiliqiangxin group and metoprolol group.Rats in Qiliqiangxin group were administered with 1 g/kg of Qiliqiangxin crude drug for 6 weeks, while rats in metoprolol group were administered with 10 mg/kg of metoprolol for 6 weeks. Rats in normaol control group and heart failure group received an equivalent volume of 0.9% saline alone intragastric administration for 6 weeks, too. Heart function of rats of all groups was detected with echocardiogram, and serum levels of tumor necrosis factor-α (TNF-α )and B-type natriuretic peptide (BNP) were detected by ELSIA. The myocardium pathological change of all groups was analyzed by histological hematoxylin and eosin staining.Result:Compared with normal control group, left ventricular end-systolic dimension(LVESD) and left ventricular end-diastolic dimension(LVEDD) were significantly increased in heart failure group (P<0.01 and P<0.05), left ventricular ejection fraction(LVEF) and shortening fraction(FS) were significantly reduced in heart failure group (P<0.01, respectively); serum levels of TNF-α and BNP significantly rose in heart failure group (P<0.01, respectively). Compared with heart failure group, LVESD, LVEDD, LVEF% and %FS were all significantly improved in metoprolol group (P<0.05, respectively); serum levels of BNP descended significantly in metoprolol group (P<0.05). Compared with heart failure group, LVEF% and %FS were significantly improved in Qiliqiangxin group(P<0.05, respectively); serum levels of TNF-α descentded significantly in Qiliqiangxin group (P<0.01). Compared Qiliqiangxin group with metoprolol group, there was no signi-ficant difference in heart function between the two groups (P>0.05, respectively); however, serum levels of BNP and TNF-α of the two groups were significantly distinct (P<0.05 and P<0.01). Histological hematoxylin and eosin staining of myocardium found as follows: There was myocardial necrosis partly in heart failure group. Mass of inflammatory cell infiltrated in the myocardium of metoprolol group. Small amounts of inflammatory cell infiltrated in the myocardium of Qiliqiangxin group. Conclusion:Qiliqiangxin capsule can improve heart function and decrease serum level of TNF-α and relieve inflammatory cell infiltration of myocardium in rats with adriamycin induced cardiomyopathy.
