北京体育大学学报
北京體育大學學報
북경체육대학학보
Journal of Beijing University of Physical Education
2012年
11期
61~64
,共null页
朱英伟 张晶 毛毅钢 徐涛
硃英偉 張晶 毛毅鋼 徐濤
주영위 장정 모의강 서도
运动性心肌肥厚 细胞微管 细胞骨架 心肌重塑 心功能 运动员心脏综合症 全心指数 左心指数
運動性心肌肥厚 細胞微管 細胞骨架 心肌重塑 心功能 運動員心髒綜閤癥 全心指數 左心指數
운동성심기비후 세포미관 세포골가 심기중소 심공능 운동원심장종합증 전심지수 좌심지수
exercise induced myocardial hypertrophy ; microtubules ; cytoskeleton ; cardiac remodeling; cardiacfunction;athletic heart syndrome; cardiac index; left cardiac index
目的：研究运动性心肌肥厚引起的心肌细胞骨架重组与心功能改变之间的关系。方法：跑台法制备大鼠运动性心肌肥厚模型。大鼠分为正常对照组、训练8周组、训练12周组及训练12周停训8周组；检测各组血流动力学指标评价心功能；测定全心指数、左心指数评价心脏肥厚程度；酶法急性分离技术制备活体单个心肌细胞，免疫荧光法对活细胞的骨架主要成分微管进行染色，在激光共聚焦显微镜下比较重组前后细胞骨架形态的差异，并读取荧光强度对a-微管进行定量测定。结果：与A组比较，B、C两组HMI及LVM增加，HR减慢，LVSP、±dp／dmax，均有升高，LVEDP降低；B、C两组进行比较，HR、LVSP及LVEDP差异无统计学意义，C组±dp／dmax高于B组；两组细胞骨架发生了重组，微管数量增多，排列紧密，亮度明显较强，C组微管量高于B组。结论：运动性心肌肥厚引起了心功能的改变，心肌细胞骨架发生重组，重组后的细胞骨架排列紧密，微管含量增加，微管对心肌细胞的弹性强度起负调节作用，而对心肌黏性强度的负调节作用不明显。
目的：研究運動性心肌肥厚引起的心肌細胞骨架重組與心功能改變之間的關繫。方法：跑檯法製備大鼠運動性心肌肥厚模型。大鼠分為正常對照組、訓練8週組、訓練12週組及訓練12週停訓8週組；檢測各組血流動力學指標評價心功能；測定全心指數、左心指數評價心髒肥厚程度；酶法急性分離技術製備活體單箇心肌細胞，免疫熒光法對活細胞的骨架主要成分微管進行染色，在激光共聚焦顯微鏡下比較重組前後細胞骨架形態的差異，併讀取熒光彊度對a-微管進行定量測定。結果：與A組比較，B、C兩組HMI及LVM增加，HR減慢，LVSP、±dp／dmax，均有升高，LVEDP降低；B、C兩組進行比較，HR、LVSP及LVEDP差異無統計學意義，C組±dp／dmax高于B組；兩組細胞骨架髮生瞭重組，微管數量增多，排列緊密，亮度明顯較彊，C組微管量高于B組。結論：運動性心肌肥厚引起瞭心功能的改變，心肌細胞骨架髮生重組，重組後的細胞骨架排列緊密，微管含量增加，微管對心肌細胞的彈性彊度起負調節作用，而對心肌黏性彊度的負調節作用不明顯。
목적：연구운동성심기비후인기적심기세포골가중조여심공능개변지간적관계。방법：포태법제비대서운동성심기비후모형。대서분위정상대조조、훈련8주조、훈련12주조급훈련12주정훈8주조；검측각조혈류동역학지표평개심공능；측정전심지수、좌심지수평개심장비후정도；매법급성분리기술제비활체단개심기세포，면역형광법대활세포적골가주요성분미관진행염색，재격광공취초현미경하비교중조전후세포골가형태적차이，병독취형광강도대a-미관진행정량측정。결과：여A조비교，B、C량조HMI급LVM증가，HR감만，LVSP、±dp／dmax，균유승고，LVEDP강저；B、C량조진행비교，HR、LVSP급LVEDP차이무통계학의의，C조±dp／dmax고우B조；량조세포골가발생료중조，미관수량증다，배렬긴밀，량도명현교강，C조미관량고우B조。결론：운동성심기비후인기료심공능적개변，심기세포골가발생중조，중조후적세포골가배렬긴밀，미관함량증가，미관대심기세포적탄성강도기부조절작용，이대심기점성강도적부조절작용불명현。
objective ： Research the relationship between the changes on exercise myocardial hypertrophy of myocar dial cells caused skeleton restructuring and heart function. Methods ： Run a method manufactured a model of rats exercise myocardial hypertrophy. Rats were divided into normal group, 8 weeks training group, 12 weeks training group and 12 weeks training and 8 weeks suspension group. The researchers detected each hemodynamic for evalu ating heart function, tested the whole heart index, left heart index to evaluate cardiac hypertrophy degree, made live single myocardial cells by enzymatic acute separate technology, dyed the microtubules of the skeleton of living cells by the method of immunofluorescence, compared cytoskeleton shape of differences of cells restructuring be fore and after under the confocal laser microscope, and read fluorescence intensity to measure the a-microtubules quantitatively. Results： Compared with group A, group B and C witnessed increased in HMI and LVM, LVSP, ± dp/dtmaX of and decrease in HR and LVEDP ; the differences about HR, LVS and LVEDP were no statistical signif icance in group B and C, group C were higher than group B in ±dp/dt cytoskeleton happened restructuring in two groups, the number of microtubules had increased, arranged close together, gained stronger brightness. The total of microtubules of group C were higher than B. Conclusions ： Exercise induced myocardial hypertrophy caused the change of heart function. Cytoskeleton of myocardial cells have restructured. Cytoskeleton arranged close to gether after reorganization. Microtubules purity increased. The microtubules had negative regulation effect on the elastic strength of myocardial cells, whereas the negative regulation was unconspicuous on myocardial adhesive strength.
