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用 TAS 定量研究了培养心肌细胞缺氧后,心肌的细胞化学、形态学和功能改变以及1,6-二磷酸果糖的作用。结果表明,心肌细胞缺氧后,LDH 活性呈先高后低的双相改变,SDH活性的降低早于 LDH 活性的改变且较严重,线粒体明显肿胀,当肿胀至其自身大小的一倍时,裂解破坏增多。FDP 可显著改善心肌细胞的 SDH 和 LDH 活性,减轻心肌细胞和线粒体肿胀,并可改善心肌细胞功能。
Tissue cytochemistry, morphological and functional changes, and the effect of fructose 1,6-diphosphate were studied quantitatively using TAS after cardiomyocyte hypoxia. The results showed that after hypoxia, the activity of LDH changed first and then decreased, and the decrease of SDH activity was earlier than the change of LDH activity and was more serious. The mitochondria obviously swollen. When swelling to one times of its own size, Cracking damage increased. FDP can significantly improve myocardial SDH and LDH activity, reduce myocardial cells and mitochondria swelling, and can improve myocardial cell function.