摘要
目的：探讨烧伤后心肌细胞膜损伤的机制。方法：采用体外心肌细胞培养模型，研究缺氧、烧伤血清对心肌细胞活力、细胞膜脂质过氧化、细胞膜脂流动性的影响。结果：单纯缺氧、单纯烧伤血清损伤６ｈ心肌细胞活力明显下降（Ｐ＜０．０１），而缺氧加烧伤血清损伤３ｈ心肌细胞活力则明显下降（Ｐ＜０．０１）。单纯缺氧损伤３ｈＭＤＡ含量增加（Ｐ＜０．０５）。单纯烧伤血清损伤６ｈＭＤＡ含量增加（Ｐ＜０．０１）。缺氧加烧伤血清损伤３、６ｈＭＤＡ含量增加（Ｐ均＜０．０１）。单纯缺氧损伤３ｈ和缺氧加烧伤血清损伤１ｈ，心肌细胞膜荧光偏振度、微粘度和分子排列有序性系数即出现增加（Ｐ＜０．０５～０．０１）。结论：缺氧、烧伤血清对心肌细胞的损伤可能与膜脂质过氧化增强有关，从而导致心肌细胞膜脂流动性降低，细胞从相对比较流动变为相对固化。
Objective: To explore the mechanism of myocardial cell membrane injury after burns. Methods: The myocardial cells were cultured and injured with hypoxia and burn serum. The changes in the viability of the cells and the membranous lipid peroxidation and fluidity were observed. Results: The viability of the myocardial cells was significantly decreased at the 6th h after being injured with hypoxia or burn serum alone and at the 3rd h after being injured with the two in combination. The content of malondialdehyde (MDA) in the cells was significantly increased at the 3rd h after being injured with hypoxia alone or hypoxia and burn serum in combination and at the 6th h after being injured with burn serum alone. The membrane polarization and microviscocity of membrane bilayer were significantly increased at the 3rd h after the cells were injured with hypoxia alone and at the 1st h with hypoxia and burn serum in combination. Conclusion: The damage of myocardial cells is related to the membrane lipid peroxidation resulting in reduction of membrane fluidity. The membrane of myocardial cells changes from a relatively fluid state to relatively solid one after being injured with hypoxia and burn serum.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1999年第2期75-77,共3页
Journal of Third Military Medical University
基金
国家自然科学基金
