心气虚大鼠自由基损伤及心肌超微结构观察

1、心气虚大鼠自由基损伤及心肌超微结构观察                        作者：唐烨霞 程志清 姚立 吴玉芙 龚文波【摘要】  目的：观察心气虚大鼠自由基损伤及心肌超微结构。方法：成年近交系Wistar大鼠26只,雌雄各半，随机分为对照组12只和观察组14只；将观察组动物制成心气虚模型后测定血清超氧化物歧化酶（SOD）和丙二醛（MDA）含量，并用

2、透射电镜观察大鼠心肌超微结构。结果：观察组SOD低于对照组(P0.01)，MDA高于对照组(P0.01)；观察组心肌细胞受到损害，肌纤维排列紊乱，线粒体肿胀，结构模糊，嵴有溶解现象。结论：心肌超微结构受损可能是导致心气虚的原因，而其损伤机制可能与自由基有关。 【关键词】  心气虚；自由基；心肌超微结构    Abstract  Objective: To observe the damage to free radical and ultramicrostructure of heart muscle in the rats with defi

3、ciency of heart-energy. Methods: 26 adult inbreeding line Wistar rats were divided into the control group (12 rats) and the model group (14 rats). After preparing animal model of deficiency of heart-energy with the rats from the model group. SOD and MDA was measured, and heart muscle ultramicrostruc

4、ture was observed as well by electron microscope. Results: SOD of swimming model group was lower than that in the control group(P0.01). MDA of swimming model group was higher than that in the   control group(P0.01). ultramicrostructure of heart muscle was damaged in the rats from the model

5、 group. Conclusion: The damage to heart muscle ultramicrostructure may be chiefly responsible fro deficiency of heart-energy, and its damaging mechanism seems to be related to free radical.    Key words  Deficiency of heart-energy； Free radical; Heart muscle ultramicrostructure&#

6、160;   目前，心血管病发病率、病死率居国内第一、二位，如何提高其疗效已成为医学界共同关注的问题。在心血管病系统中，心气虚证为常见证型1。因此，对心气虚证研究是中医防治心血管疾病的关键。如果能探寻导致心气虚证的原因，就会为心气虚证的防治带来新的思路和方法。我们在成功制备了不含其它兼证的心气虚证动物模型的基础上，探寻心气虚证与自由基损伤及心肌超微结构的关系，以期寻找导致心气虚证的机理。    1  材料与方法    1.1  实验材料    1.2  实

7、验方法1         【摘要】  目的：观察心气虚大鼠自由基损伤及心肌超微结构。方法：成年近交系Wistar大鼠26只,雌雄各半，随机分为对照组12只和观察组14只；将观察组动物制成心气虚模型后测定血清超氧化物歧化酶（SOD）和丙二醛（MDA）含量，并用透射电镜观察大鼠心肌超微结构。结果：观察组SOD低于对照组(P0.01)，MDA高于对照组(P0.01)；观察组心肌细胞受到损害，肌纤维排列紊乱，线粒体肿胀，结构模糊，嵴有溶解现象。结论：心肌超微结构受损可能是导致心气虚的原因，而其损伤机制可能与自由基

8、有关。 【关键词】  心气虚；自由基；心肌超微结构Observation of the Damage to Free Radical and Heart Muscle Ultramicrostructure in    the Rats with Deficiency of Heart-energy    TANG Yexia,CHENG Zhiqing,YAO Li,et al    (Department of Physiology ,Baotou Medical College,Baoto

9、u 014060,China)    Abstract  Objective: To observe the damage to free radical and ultramicrostructure of heart muscle in the rats with deficiency of heart-energy. Methods: 26 adult inbreeding line Wistar rats were divided into the control group (12 rats) and the model group (14 r

10、ats). After preparing animal model of deficiency of heart-energy with the rats from the model group. SOD and MDA was measured, and heart muscle ultramicrostructure was observed as well by electron microscope. Results: SOD of swimming model group was lower than that in the control group(P0.01). MDA o

11、f swimming model group was higher than that in the   control group(P0.01). ultramicrostructure of heart muscle was damaged in the rats from the model group. Conclusion: The damage to heart muscle ultramicrostructure may be chiefly responsible fro deficiency of heart-energy, and its damagin

12、g mechanism seems to be related to free radical.    Key words  Deficiency of heart-energy； Free radical; Heart muscle ultramicrostructure    目前，心血管病发病率、病死率居国内第一、二位，如何提高其疗效已成为医学界共同关注的问题。在心血管病系统中，心气虚证为常见证型1。因此，对心气虚证研究是中医防治心血管疾病的关键。如果能探寻导致心气虚证的原因，就会为心气虚证的防治带来新的思路和方法。我

13、们在成功制备了不含其它兼证的心气虚证动物模型的基础上，探寻心气虚证与自由基损伤及心肌超微结构的关系，以期寻找导致心气虚证的机理。    1  材料与方法    1.1  实验材料    1.2  实验方法    2  结果    2.1  生化指标  观察组SOD含量低于对照组(P0.01)，造模组MDA含量高于对照组(P0.01)，观察组cAMP含量低于对照组(P0.01)。见表1。表

14、1  Wistar大鼠游泳组生化指与正常组比较*与正常组比较P0.05，*与正常组比较P0.01    2.2  形态学改变  心肌光镜检查未发现明显的结构变化。电镜结果显示，观察组大鼠心肌细胞肌原纤维排列紊乱，线粒体肿胀，结构模糊，嵴有溶解现象。见图1。3  讨论    实验中观察组动物血清SOD含量均明显下降(P0.01)，MDA含量升高，与临床心气虚患者SOD含量明显低于健康人（P0.05）一致。这是由于心气虚证机体抗氧化作用减弱，对脂质过氧化物清除能力减弱，而导致生物体的自由基代谢的动态平衡失调3。    环核苷酸信号系统主要由cAMP和才cGMP两个相对独立系统组成，cAMP在细胞外信息分子调节细胞功能的过程中，起着快速跨膜传递和广大信号的作用。cGMP浓度一般比cAMP低，其介导的作用常与cAMP相反4。观察