中国医药
中國醫藥
중국의약
CHINA MEDICINE
2009年
9期
655-658
,共4页
何华%高玖鸣%王文%王佩合%张铭%贾平
何華%高玖鳴%王文%王珮閤%張銘%賈平
하화%고구명%왕문%왕패합%장명%가평
慢性心力衰竭%大鼠%腹主动脉缩窄%心肌肥厚
慢性心力衰竭%大鼠%腹主動脈縮窄%心肌肥厚
만성심력쇠갈%대서%복주동맥축착%심기비후
Chronic heart failure%Rat%Abdominal aortic constriction%Myocardial hypertrophy
目的 探讨压力负荷型心肌肥厚(POH)、肥厚逆转和慢性心力衰竭(CHF)大鼠模型的建立及其评价体系.方法 8周龄SD雄性大鼠100只编码后按4:1比例分为2组:腹主动脉缩窄(AAC)组(80例)和假手术组(20例),分别行肾上腹主动脉缩窄术或假手术.术后12周,根据超声左心室质量/体质量,AAC组进一步分为心肌肥厚组、肥厚逆转组、心衰组,分别给予正常饮食、福辛普利和卡维地洛灌胃、高盐饮食.结果 超声、血流动力学、心质量/体质量、组织形态学等方面证据表明假手术组未发生心肌肥厚和心衰,心肌肥厚组出现明显心肌肥厚,肥厚逆转组表现为心肌肥厚的逆转心衰组则建立了明确的心衰.结论 采用AAC法可以建立大鼠POH模型,血管紧张素转换酶抑制剂与β阻滞剂合用可明显恢复POH模型的肥厚心肌而形成肥厚逆转模型,在钠负荷下可促使POH进展为CHF而形成CHF模型.用超声心动图、血流动力学、心肺重量指数、光镜下心肺组织形态学证据结合症状观察,能较好地识别大鼠的心肌肥厚和CHF.
目的 探討壓力負荷型心肌肥厚(POH)、肥厚逆轉和慢性心力衰竭(CHF)大鼠模型的建立及其評價體繫.方法 8週齡SD雄性大鼠100隻編碼後按4:1比例分為2組:腹主動脈縮窄(AAC)組(80例)和假手術組(20例),分彆行腎上腹主動脈縮窄術或假手術.術後12週,根據超聲左心室質量/體質量,AAC組進一步分為心肌肥厚組、肥厚逆轉組、心衰組,分彆給予正常飲食、福辛普利和卡維地洛灌胃、高鹽飲食.結果 超聲、血流動力學、心質量/體質量、組織形態學等方麵證據錶明假手術組未髮生心肌肥厚和心衰,心肌肥厚組齣現明顯心肌肥厚,肥厚逆轉組錶現為心肌肥厚的逆轉心衰組則建立瞭明確的心衰.結論 採用AAC法可以建立大鼠POH模型,血管緊張素轉換酶抑製劑與β阻滯劑閤用可明顯恢複POH模型的肥厚心肌而形成肥厚逆轉模型,在鈉負荷下可促使POH進展為CHF而形成CHF模型.用超聲心動圖、血流動力學、心肺重量指數、光鏡下心肺組織形態學證據結閤癥狀觀察,能較好地識彆大鼠的心肌肥厚和CHF.
목적 탐토압력부하형심기비후(POH)、비후역전화만성심력쇠갈(CHF)대서모형적건립급기평개체계.방법 8주령SD웅성대서100지편마후안4:1비례분위2조:복주동맥축착(AAC)조(80례)화가수술조(20례),분별행신상복주동맥축착술혹가수술.술후12주,근거초성좌심실질량/체질량,AAC조진일보분위심기비후조、비후역전조、심쇠조,분별급여정상음식、복신보리화잡유지락관위、고염음식.결과 초성、혈류동역학、심질량/체질량、조직형태학등방면증거표명가수술조미발생심기비후화심쇠,심기비후조출현명현심기비후,비후역전조표현위심기비후적역전심쇠조칙건립료명학적심쇠.결론 채용AAC법가이건립대서POH모형,혈관긴장소전환매억제제여β조체제합용가명현회복POH모형적비후심기이형성비후역전모형,재납부하하가촉사POH진전위CHF이형성CHF모형.용초성심동도、혈류동역학、심폐중량지수、광경하심폐조직형태학증거결합증상관찰,능교호지식별대서적심기비후화CHF.
Objective To develop pressure-overloaded myocardial hypertrophy, hypertrophy-reverse and chronic heart failure models and to form an assessing system for the 3 kinds of models. Methods Eight-week-old Sprague-Dawley rats were divided into abdominal aortic constriction (AAC) group and sham group. AAC group was further divided into three groups according to echocardiograph index LVmass/BW at 12 weeks after surgery: myocar-dial hypertrophy without failure (POH-NF), hypertrophy-reverse (POH-Re) and heart failure (POH-F) group, which respectively received normal diet for 4 weeks and were treated with Carvedilol and Fosinopril for 8 weeks and high-salt diet for 12 weeks. Hemodynamic parameters were examined and cardiac contractile function was assessed through cardiocatheter via carotid artery before euthanasia. Hearts and lungs of rats were weighed and part of tissue of hearts and lungs was prepared for histomorphological analysis. Results Compared with sham group, echocardio-graph index end-diastolic ventricular septal thickness (IVSd), end-diastolic ventricular posterior wall thickness (LVPWd), left ventricular mass(LVmass) of POH-NF group and IVSd, LVPWd, LVmass, left ventricular end-di-astolic diameter (LVIDd), left ventricular end-systolic diameter(LVIDs) of POH-F group increased, whereas frac-tional endocardial shortening(FS), ejection fraction(EF) of POH-F group decreased. LVPWd, LVmaas of POH-Re group after administration were not significantly different from these of sham group. Basal hemodynamic parameters HR, SBP, left ventricular end-systolic pressure (LVESP) and maximum value of the first derivative of the ventricu-lar pressure wave(dp/dtmax) of POH-NF group increased. SBP, LVESP of POH-Re group recovered. Elevated left ventricular end-diastolic pressure (LVEDP) and decreased dp/dtmax were found in POH-F group. HW,HW/BW of POH-NF and POH-F group significantly increased. LW,LW/BW of POH-F group also increased. (all P <0.05 ).There were significant myocardial disarray, myocardial hypertrophy and enlarged, strange, densely stained cell nuclear in hearts of POH-NF. Significant lung congestion was found in POH-F group. Conclusion POH model was established by AAC. Angiotension converting enzyme inhibitors combined with 13-blocker could significantly reverse hypertrophic myocardium in POH model to reform a POH-Re model. Meanwhile, it could promote POH to chronic heart failure to reform a CHF model. Combination of manifestations, echocardiography, hemodynamics, weight index of heart, lung and histological observation of heart and lung can set up an assessing system that distinguishes the myocardial hypertrophy in rat CHF models.