目的 动态观察低硒对大鼠在体心功能及线粒体超微结构的影响,探讨低硒致心肌损伤的机制.方法 断乳2周清洁级SD大鼠48只,按体质量随机分为低硒(LS)组和对照(NC)组,每组24只,雌雄各半.对照组给予常规饲料(硒含量0.10～ 0.30 mg/kg)喂养,低硒组给予人工合成低硒饲料(硒含量0.01 mg/kg)喂养.两组大鼠分别在喂养10、20、30、40周后,各选取6只,雌雄各半,2,3-二氨基奈荧光法检测血硒水平；颈动脉插管检测大鼠在体心功能；电子天平称心脏重量；透射电镜下观察心肌线粒体的超微结构并用体视学方法对线粒体结构的变化情况进行定量分析.结果 与NC组比较[(0.421±0.076)、(0.409±0.057)、(0.416±0.033)、(0.386±0.050)mg/L],LS组大鼠喂养10、20、30、40周后血硒降低[(0.102±0.018)、(0.053±0.012)、(0.045±0.014)、(0.027±0.008) mg/L,P均＜0.05].大鼠喂养到20、30、40周时,LS组左心室峰值收缩压(LVSP)[(113.30±2.21)、(103.82±5.24)、(97.74±2.87)mm Hg,1 mm Hg=0.133 kPa]和左心室内压最大上升速率(+dp/dtmax)[(7366.10±455.61)、(6160.68±402.17)、(5381.21±646.72)mm Hg· s-1]均明显低于相应NC组[(130.30±3.72)、(118.97±5.31)、(120.08±3.29)mm Hg,(10 430.00±808.56)、(8582.62±621.14)、(8295.88±1318.29)mm Hg·s-1,P均＜0.05],且LVSP和+dp/dtmax均随低硒喂养时间延长而逐渐减低(P均＜ 0.05).大鼠喂养到20、30、40周时,LS组心脏与体质量之比(HW/BW×100,0.2859±0.0081、0.2948±0.0171、0.2949±0.0056)、左心室与体质量之比(LVW/BW×100,0.2302±0.0041、0.2387±0.0131、0.2386±0.0024)、左心室与心脏重量之比(LVW/HW,0.8063±0.0122、0.8104±0.0031、0.8098±0.0109)均高于NC组(0.2798±0.0103、0.2761±0.0128、0.2718±0.0051,0.2185±0.0094、0.2145±0.0131、0.2123±0.0027,0.7813±0.0210、0.7751±0.0165、0.7815±0.0100,P均＜0.05).电镜观察可见LS组大鼠心肌线粒体嵴膜减少,线粒体明显肿胀；体视学检测大鼠在喂养到10、20、30、40周时,LS组体密度(Vv)[(0.3108±0.0053)％、(0.3286±0.0036)％、(0.3877±0.0211)％、(0.3990±0.0115)％]和面密度(Sv)[(0.0284±0.0002)、(0.0295±0.0007)、(0.0338±0.0026)、(0.0332±0.0004) μm-1]高于NC组[(0.2402±0.0143)％、(0.2375±0.0241)％、(0.2657±0.0239)％、(0.2892±0.0302)％,(0.0231±0.0015)、(0.0221±0.0019)、(0.0241±0.0014)、(0.0273±0.0028)μm-1,P均＜ 0.05]；在20、30、40周时,LS组比表面积(Rsv)[(0.0899±0.0015)、(0.0868±0.0031)、(0.0835±0.0013)μm-1]低于NC组[(0.0939±0.0020)、(0.0915±0.0023)、(0.0946±0.0021)μm-1,P均＜0.05].相关性分析显示,Rsv分别与LVSP和+dp/dtmax相关(r值分别为0.508、0.502,P均＜0.01).结论 低硒可导致大鼠心肌线粒体超微结构异常,并导致心脏功能发生变化,以收缩功能损伤更为明显；线粒体的损伤与心功能减退具有相关性；线粒体在低硒致心功能受损过程中发挥重要作用.
目的 動態觀察低硒對大鼠在體心功能及線粒體超微結構的影響,探討低硒緻心肌損傷的機製.方法 斷乳2週清潔級SD大鼠48隻,按體質量隨機分為低硒(LS)組和對照(NC)組,每組24隻,雌雄各半.對照組給予常規飼料(硒含量0.10～ 0.30 mg/kg)餵養,低硒組給予人工閤成低硒飼料(硒含量0.01 mg/kg)餵養.兩組大鼠分彆在餵養10、20、30、40週後,各選取6隻,雌雄各半,2,3-二氨基奈熒光法檢測血硒水平；頸動脈插管檢測大鼠在體心功能；電子天平稱心髒重量；透射電鏡下觀察心肌線粒體的超微結構併用體視學方法對線粒體結構的變化情況進行定量分析.結果 與NC組比較[(0.421±0.076)、(0.409±0.057)、(0.416±0.033)、(0.386±0.050)mg/L],LS組大鼠餵養10、20、30、40週後血硒降低[(0.102±0.018)、(0.053±0.012)、(0.045±0.014)、(0.027±0.008) mg/L,P均＜0.05].大鼠餵養到20、30、40週時,LS組左心室峰值收縮壓(LVSP)[(113.30±2.21)、(103.82±5.24)、(97.74±2.87)mm Hg,1 mm Hg=0.133 kPa]和左心室內壓最大上升速率(+dp/dtmax)[(7366.10±455.61)、(6160.68±402.17)、(5381.21±646.72)mm Hg· s-1]均明顯低于相應NC組[(130.30±3.72)、(118.97±5.31)、(120.08±3.29)mm Hg,(10 430.00±808.56)、(8582.62±621.14)、(8295.88±1318.29)mm Hg·s-1,P均＜0.05],且LVSP和+dp/dtmax均隨低硒餵養時間延長而逐漸減低(P均＜ 0.05).大鼠餵養到20、30、40週時,LS組心髒與體質量之比(HW/BW×100,0.2859±0.0081、0.2948±0.0171、0.2949±0.0056)、左心室與體質量之比(LVW/BW×100,0.2302±0.0041、0.2387±0.0131、0.2386±0.0024)、左心室與心髒重量之比(LVW/HW,0.8063±0.0122、0.8104±0.0031、0.8098±0.0109)均高于NC組(0.2798±0.0103、0.2761±0.0128、0.2718±0.0051,0.2185±0.0094、0.2145±0.0131、0.2123±0.0027,0.7813±0.0210、0.7751±0.0165、0.7815±0.0100,P均＜0.05).電鏡觀察可見LS組大鼠心肌線粒體嵴膜減少,線粒體明顯腫脹；體視學檢測大鼠在餵養到10、20、30、40週時,LS組體密度(Vv)[(0.3108±0.0053)％、(0.3286±0.0036)％、(0.3877±0.0211)％、(0.3990±0.0115)％]和麵密度(Sv)[(0.0284±0.0002)、(0.0295±0.0007)、(0.0338±0.0026)、(0.0332±0.0004) μm-1]高于NC組[(0.2402±0.0143)％、(0.2375±0.0241)％、(0.2657±0.0239)％、(0.2892±0.0302)％,(0.0231±0.0015)、(0.0221±0.0019)、(0.0241±0.0014)、(0.0273±0.0028)μm-1,P均＜ 0.05]；在20、30、40週時,LS組比錶麵積(Rsv)[(0.0899±0.0015)、(0.0868±0.0031)、(0.0835±0.0013)μm-1]低于NC組[(0.0939±0.0020)、(0.0915±0.0023)、(0.0946±0.0021)μm-1,P均＜0.05].相關性分析顯示,Rsv分彆與LVSP和+dp/dtmax相關(r值分彆為0.508、0.502,P均＜0.01).結論 低硒可導緻大鼠心肌線粒體超微結構異常,併導緻心髒功能髮生變化,以收縮功能損傷更為明顯；線粒體的損傷與心功能減退具有相關性；線粒體在低硒緻心功能受損過程中髮揮重要作用.
목적 동태관찰저서대대서재체심공능급선립체초미결구적영향,탐토저서치심기손상적궤제.방법 단유2주청길급SD대서48지,안체질량수궤분위저서(LS)조화대조(NC)조,매조24지,자웅각반.대조조급여상규사료(서함량0.10～ 0.30 mg/kg)위양,저서조급여인공합성저서사료(서함량0.01 mg/kg)위양.량조대서분별재위양10、20、30、40주후,각선취6지,자웅각반,2,3-이안기내형광법검측혈서수평；경동맥삽관검측대서재체심공능；전자천평칭심장중량；투사전경하관찰심기선립체적초미결구병용체시학방법대선립체결구적변화정황진행정량분석.결과 여NC조비교[(0.421±0.076)、(0.409±0.057)、(0.416±0.033)、(0.386±0.050)mg/L],LS조대서위양10、20、30、40주후혈서강저[(0.102±0.018)、(0.053±0.012)、(0.045±0.014)、(0.027±0.008) mg/L,P균＜0.05].대서위양도20、30、40주시,LS조좌심실봉치수축압(LVSP)[(113.30±2.21)、(103.82±5.24)、(97.74±2.87)mm Hg,1 mm Hg=0.133 kPa]화좌심실내압최대상승속솔(+dp/dtmax)[(7366.10±455.61)、(6160.68±402.17)、(5381.21±646.72)mm Hg· s-1]균명현저우상응NC조[(130.30±3.72)、(118.97±5.31)、(120.08±3.29)mm Hg,(10 430.00±808.56)、(8582.62±621.14)、(8295.88±1318.29)mm Hg·s-1,P균＜0.05],차LVSP화+dp/dtmax균수저서위양시간연장이축점감저(P균＜ 0.05).대서위양도20、30、40주시,LS조심장여체질량지비(HW/BW×100,0.2859±0.0081、0.2948±0.0171、0.2949±0.0056)、좌심실여체질량지비(LVW/BW×100,0.2302±0.0041、0.2387±0.0131、0.2386±0.0024)、좌심실여심장중량지비(LVW/HW,0.8063±0.0122、0.8104±0.0031、0.8098±0.0109)균고우NC조(0.2798±0.0103、0.2761±0.0128、0.2718±0.0051,0.2185±0.0094、0.2145±0.0131、0.2123±0.0027,0.7813±0.0210、0.7751±0.0165、0.7815±0.0100,P균＜0.05).전경관찰가견LS조대서심기선립체척막감소,선립체명현종창；체시학검측대서재위양도10、20、30、40주시,LS조체밀도(Vv)[(0.3108±0.0053)％、(0.3286±0.0036)％、(0.3877±0.0211)％、(0.3990±0.0115)％]화면밀도(Sv)[(0.0284±0.0002)、(0.0295±0.0007)、(0.0338±0.0026)、(0.0332±0.0004) μm-1]고우NC조[(0.2402±0.0143)％、(0.2375±0.0241)％、(0.2657±0.0239)％、(0.2892±0.0302)％,(0.0231±0.0015)、(0.0221±0.0019)、(0.0241±0.0014)、(0.0273±0.0028)μm-1,P균＜ 0.05]；재20、30、40주시,LS조비표면적(Rsv)[(0.0899±0.0015)、(0.0868±0.0031)、(0.0835±0.0013)μm-1]저우NC조[(0.0939±0.0020)、(0.0915±0.0023)、(0.0946±0.0021)μm-1,P균＜0.05].상관성분석현시,Rsv분별여LVSP화+dp/dtmax상관(r치분별위0.508、0.502,P균＜0.01).결론 저서가도치대서심기선립체초미결구이상,병도치심장공능발생변화,이수축공능손상경위명현；선립체적손상여심공능감퇴구유상관성；선립체재저서치심공능수손과정중발휘중요작용.
Objective To dynamically observe the cardiac function in vivo and ultrastructure of myocardial mitochondria in selenium deficiency rats so as to provide a theoretical basis for revealing the mechanism of myocardial injury induced by selenium deficiency.Methods Forty eight of two-week old SD rats were randomly divided into low-selenium(LS) group and normal control(NC) group,24 rats in each group(female 12,male 12).Normal group was fed with Se-normal food (selenium content 0.10-0.30 mg/kg),low-selenium group was fed with Se-deficient food(selenium content 0.01 mg/kg).At four time points(10 w,20 w,30 w and 40 w) the following were done:fluorometric determination of whole blood Se levels with 2,3-diaminonaphthalene;measuring hemodynamics in vivo and cardiac weight; transmission electron microscope(TEM) observation of mitochondrial ultrastructure and quantitative analysis of mitochondrial structure changes using stereological methods.Results After feeding for 10,20,30 and 40 weeks,the blood selenium level of LS group[(0.102 ± 0.018),(0.053 ± 0.012),(0.045 ± 0.014),(0.027 ± 0.008)mg/L] decreased significantly compared with NC group[(0.421 ± 0.076),(0.409 ± 0.057),(0.416 ± 0.033),(0.386 ± 0.050)mg/L,all P ＜ 0.05].When the rats were fed for 20,30 and 40 weeks,the left ventricular systolic pressure (LVSP) [(113.30 ± 2.21),(103.82 ± 5.24),(97.74 ± 2.87) mm Hg,1 mm Hg =0.133 kPa]and maximum rate of rise of left ventricular pressure (+dp/dtmax) [(7366.10 ± 455.61),(6160.68 ± 402.17),(5381.21 ± 646.72)mm Hg·s-1] of LS group decreased significantly compared with NC group[(130.30± 3.72)mm Hg,(118.97 ± 5.31)mm Hg,(120.08 ± 3.29)mm Hg,(10 430.00 ± 808.56)mm Hg·s-1,(8582.62 ± 621.14) mm Hg·s-1,(8295.88± 1318.29)mm Hg·s-1,all P＜ 0.05],and the reduction gradually reduced with prolonged feeding with low selenium(all P ＜ 0.05).The heart weight(HW)/body weight(BW) ratio × 100(0.2859 ± 0.0081,0.2948 ± 0.0171,0.2949 ± 0.0056),left ventricular weight(LVW)/BW ratio × 100(0.2302 ± 0.0041,0.2387 ± 0.0131,0.2386 ± 0.0024) and LVW/HW ratio(0.8063 ± 0.0122,0.8104 ± 0.0031,0.8098 ± 0.0109) of LS group were significantly higher than those in NC group(0.2798 ± 0.0103,0.2761 ± 0.0128,0.2718 ± 0.0051,0.2185 ± 0.0094,0.2145 ± 0.0131,0.2123 ± 0.0027,0.7813 ± 0.0210,0.7751 ± 0.0165,0.7815 ± 0.0100,all P ＜ 0.05).Observed by TEM,the cristae membrane of mitochondria reduced,and mitochondria swelled significantly.When the rats were fed for 20,30 and 40 weeks,volume density(Vv)[(0.3108 ± 0.0053)％,(0.3286 ± 0.0036)％,(0.3877 ± 0.0211)％,(0.3990 ± 0.0115)％] and surface density(Sv) [0.0284 ± 0.0002),(0.0295 ± 0.0007),(0.0338 ± 0.0026),(0.0332 ± 0.0004)μm-1] of mitochondria in LS group increased significantly,compared with those of NC group[(0.2402 ± 0.0143)％,(0.2375 ± 0.0241)％,(0.2657 ± 0.0239)％,(0.2892 ± 0.0302)％,(0.0231 ± 0.0015)μm-1,(0.0221 ± 0.0019)μm-1,(0.0241 ± 0.0014)μm-1,(0.0273 ± 0.0028)μm-1,all P＜ 0.05],and specific surface(Rsv) of LS group[(0.0899 ± 0.0015),(0.0868 ± 0.0031),(0.0835 ± 0.0013)μm-1] reduced,compared with those of NC group[(0.0939 ± 0.0020),(0.0915 ± 0.0023),(0.0946 ± 0.0021)μm-1,all P ＜ 0.05].The correlation analysis indicated that Rsv was positively correlated with LVSP and +dp/dtmax,and the correlation coefficients were 0.508 and 0.502,respectively (all P ＜ 0.01).Conclusions Selenium deficiency can lead to abnormalities of mitochondrial ultrastructure and changes in cardiac function,and among the changes of cardiac function,systolic dysfunction is more apparent.Mitochondria damage and cardiac dysfunction is correlated.Mitochondria plays an important role in cardiac dysfunction caused by selenium deficiency.
