论文部分内容阅读
为研究模拟失重大鼠心肌结构的变化，对８周悬吊大鼠用饱和ＫＣｌ溶液使心脏停搏于完全舒张状态，再行心脏原位灌注固定，以排除标本制备中缺氧及渗透压等对心肌结构的影响。用光镜与电镜对心肌的结构进行定量观察发现：与同步对照组相比，悬吊大鼠心脏重量、左右心室重量保持不变。８周悬吊大鼠左室心肌细胞的平均体积较对照组减少２３％（Ｐ＜０．０１），心肌细胞的横截面积仅呈降低趋势，差别未达显著水平（Ｐ＞０．０５），但平均长度缩短１７％（Ｐ＜０．０５）。在心肌组织中，心肌细胞与毛细血管的体密度均未改变（Ｐ＞０．０５），但悬吊组间质组织的体密度明显降低（Ｐ＜０．０１）。提示，８ｗ模拟失重可引起心肌组织萎缩。心肌细胞的萎缩是以其平均长度的缩短为特征的．
In order to study the changes of myocardial structure in simulated weightless rats, the hearts were arrested in a state of complete relaxation by saturated KCl solution for 8 weeks in suspension rats, and then fixed in situ to eliminate hypoxia and osmotic pressure Effects on Myocardial Structure. Using light microscopy and electron microscopy to quantitatively observe the structure of the myocardium, we found that compared with the synchronous control group, the weight of the heart of the suspended rat and the left and right ventricular weight remained the same. The average volume of left ventricular myocytes in the 8-week suspension rats decreased by 23% (P <0.01) compared with that in the control group, while the cross-sectional area of the cardiomyocytes showed only a decreasing trend (P> 0.05) , But the average length was shortened by 17% (P <0.05). In myocardial tissue, the density of cardiomyocytes and capillaries did not change (P> 0.05), but the density of the interstitial tissue in the suspension group was significantly decreased (P <0.01). Tip, 8w simulated weight loss can cause myocardial atrophy. Atrophy of cardiomyocytes is characterized by a shortening of their average length.