CAJ | 학술논문

目的观察亚急型克山病心肌超微结构立体学病理改变及线粒体琥珀酸脱氢酶活性变化.方法收集亚急型克山病和非心肌病(对照)组病例心肌标本,进行心肌超微结构观察;按点计数方式测量心肌线粒体体积(Vmatr)密度、嵴膜密度、体积密度;利用模型排水法测量Vmatr;用铁-铜法显示线粒体琥珀酸脱氢酶活性.结果亚急型克山病组心肌线粒体容积(Vmito)与细胞容积(Vcell)比值[(47.79±6.20)%]、线粒体面积(Smito)与肌浆面积(Splas)比值[(55.06±6.50)%]、Smito与肌原纤维面积(Smf)比值[(1.43±0.41)%]、线粒体切面面积(Sm)[(0.78±0.15)μm2]、线粒体嵴膜破坏消失区面积(Smcl)与基质面积(Smatr)、Vmatr比值[(67.14±13.96)%、(44.62±13.44)%],均明显大于对照组[(33.20±7.62)%、(38.07±9.43)%、(0.71±0.33)%、(0.44±0.07)μm2、(14.11±12.51)%、(9.34±11.28)%;t值分别为3.75、7.93、6.61、36.40、52.65、37.51,P均<0.05].亚急型克山病组心肌肌原纤维容积(Vmf)与Vcell比值[(34.52±5.12)%]、线粒体嵴膜面积(Sme)与Smatr比值[(32.43±14.42)%]明显小于对照组[(48.51±4.30)%、(86.04±12.37)%;t值分别为9.85、53.46,P均<0.05].亚急型克山病组线粒体琥珀酸脱氢酶活性多呈阴性反应.结论亚急型克山病心肌出现Smito和Vmito增大、线粒体嵴膜破坏等为主的超微结构立体学改变及线粒体琥珀酸脱氢酶活性减弱或丧失.
목적 관찰아급형극산병심기초미결구입체학병리개변급선립체호박산탈경매활성변화.방법 수집아급형극산병화비심기병(대조)조병례심기표본,진행심기초미결구관찰;안점계수방식측량심기선립체체적(Vmatr)밀도、척막밀도、체적밀도;이용모형배수법측량Vmatr;용철-동법현시선립체호박산탈경매활성.결과 아급형극산병조심기선립체용적(Vmito)여세포용적(Vcell)비치[(47.79±6.20)%]、선립체면적(Smito)여기장면적(Splas)비치[(55.06±6.50)%]、Smito여기원섬유면적(Smf)비치[(1.43±0.41)%]、선립체절면면적(Sm)[(0.78±0.15)μm2]、선립체척막파배소실구면적(Smcl)여기질면적(Smatr)、Vmatr비치[(67.14±13.96)%、(44.62±13.44)%],균명현대우대조조[(33.20±7.62)%、(38.07±9.43)%、(0.71±0.33)%、(0.44±0.07)μm2、(14.11±12.51)%、(9.34±11.28)%;t치분별위3.75、7.93、6.61、36.40、52.65、37.51,P균<0.05].아급형극산병조심기기원섬유용적(Vmf)여Vcell비치[(34.52±5.12)%]、선립체척막면적(Sme)여Smatr비치[(32.43±14.42)%]명현소우대조조[(48.51±4.30)%、(86.04±12.37)%;t치분별위9.85、53.46,P균<0.05].아급형극산병조선립체호박산탈경매활성다정음성반응.결론 아급형극산병심기출현Smito화Vmito증대、선립체척막파배등위주적초미결구입체학개변급선립체호박산탈경매활성감약혹상실.
Objective To perform a spatial analysis of myocardium uhrastructure and the activity of mitochondrial succinate dehydrogenase in sub-acute Keshan disease. Methods Myocardium samples were collected from the cases with sub-acute Keshan disease and non-myocarditis(control), and their ultrastructure was observed under electron microscope. The density of mitochondrion volume and cristal membrane and its volume were measured by a point-counting method, while mitochondrion volume was estimated by water displacement method, succinate dehydrogenase activity of mitochondrion by iron-copper method in sub-acute Keshan disease and non-myocarditis cases. Results The volume ratio of mitochondrion to the cell on myoeardium [(47.79±6.20)%], the area ratio of mitochondrion to sarcoplasm [(55.06±6.50) %], mitochondrion to myofibrils [(1.43±0,41)%], mitochondrion section area[(0.78±0.15)μm2], and ratio of the lesion of cristal membrane area to the matrix area and mitochondrion volume[(67.14±13.96)%, (44.62±13.44)%]in sub-acute Keshan disease group were obviously higher than those in control [(33.20±7.62)%, (38.07±9.43)%, (0.71±0.33)%, (0.44±0.07)μm2, (14.11± 12.51)%, (9.34±11.28)%; t = 3.75,7.93,6.61,36.40,52.65,37.51, all P < 0.05]. The volume ratio of myofibrils to cell[(34.52±5.12)%]and the area ratio of cristae mitochondria to matrix[(32.43±14.42)%]in sub-acute Keshan disease group was obviously less than those in control [(48.51±4.30)%, (86.04±12.37)%; t = 9.85, 53.46, both P < 0.05)]. Succinate dehydrogenase activity was negative in sub-acute Keshan disease group. Conclusions Myocardium ultrastructure changes in sub-acute Keshan disease including the increase of volume and areas of mitochondria and the damage of the cristal membrane in mitochondria. Succinate dehydrogenase activity is decreased or even disappeared.