CAJ | 학술논문

目的：研究衰老大鼠心肌线粒体通透性转换（ PT）孔开放对线粒体呼吸功能的影响及机制。方法左心室插管检测大鼠心功能；透射电镜检测大鼠心肌组织线粒体形态学改变；线粒体肿胀法检测心肌线粒体PT孔开放程度；氧电极法检测大鼠线粒体呼吸速率；荧光法检测线粒体膜电位。结果同3月龄组大鼠相比，15和18月龄组大鼠线粒体出现空泡肿胀、线粒体内膜脊出现断裂；大鼠左室收缩压（LVSP）和左室压上升／下降最大速率（±dp／dtmax）降低（P＜0．01）；线粒体PT孔开放幅度明显增强（P＜0．01），左室舒张末压（LVEDP）升高（P＜0．01）；线粒体膜电位下降（P＜0．01）；线粒体呼吸速率明显降低（P＜0．01）。线粒体PT孔开放抑制了线粒体呼吸功能，降低了线粒体膜电位（P＜0．01），但是抑制线粒体呼吸功能对线粒体PT孔开放和线粒体膜电位无影响（ P＞0．05）。结论衰老大鼠线粒体PT孔开放可能通过降低线粒体膜电位抑制线粒体呼吸功能。
목적：연구쇠로대서심기선립체통투성전환（ PT）공개방대선립체호흡공능적영향급궤제。방법좌심실삽관검측대서심공능；투사전경검측대서심기조직선립체형태학개변；선립체종창법검측심기선립체PT공개방정도；양전겁법검측대서선립체호흡속솔；형광법검측선립체막전위。결과동3월령조대서상비，15화18월령조대서선립체출현공포종창、선립체내막척출현단렬；대서좌실수축압（LVSP）화좌실압상승／하강최대속솔（±dp／dtmax）강저（P＜0．01）；선립체PT공개방폭도명현증강（P＜0．01），좌실서장말압（LVEDP）승고（P＜0．01）；선립체막전위하강（P＜0．01）；선립체호흡속솔명현강저（P＜0．01）。선립체PT공개방억제료선립체호흡공능，강저료선립체막전위（P＜0．01），단시억제선립체호흡공능대선립체PT공개방화선립체막전위무영향（ P＞0．05）。결론쇠로대서선립체PT공개방가능통과강저선립체막전위억제선립체호흡공능。
Objective To investigate effect of mitochondrial permeability transition ( PT) pore opening on mitochondrial respiratory function in aged rats.Methods Cardiac function was measured by inserting a tube into the left ventricle of rats.Morphological changes of hearts from rats were detected by transmission electron microscope.Mitochondrial permeability transition pore opening was measured by mito-chondrial swelling method.Mitochondrial respiratory function was measured by oxygen electrode method.Mitochondrial membrane potential was measured by fluorescence method.Results Compared with rats aged 3 months, the mitochondria in rats aged 15, 18 months was swol-len, vacuolated and the mitochondrial ridge was broken;the LVSP and ±dp/dtmax were decreased(P<0.01),LVEDP was increased (P<0.01) and mitochondrial membrane potential was decreased(P<0.01);the opening of mitochondrial permeability transition pore was inhibi-ted the respiratiory function of mitochondria and the mitochondrial membrane potential, respectively(P<0.01).However,inhibition of mito-chondrial respiratory function had no effect on opening of mitochondrial permeability transition pore and the mitochondrial membrane potential ( P>0.05) .Conclusions Opening of mitochondrial permeability transition pore could inhibit mitochondrial respiratory function via decrea-sing mitochondrial membrane potential.