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目的:探讨缺氧对血管内皮细胞(VEC)的直接损伤及影响。方法:在氧分压为3.94kPa(1kPa=7.5mmHg)低氧环境中培养人脐静脉内皮细胞(HUVEC),观察在不同时相点培养液中乳酸脱氢酶(LDH)活性、6-酮-PGF_(1α)变化和细胞内聚合肌动蛋白(F-actin)的含量与细胞形态学变化。结果:在低氧分压下1小时,培养液中 LDH 活性明显高于对照组。卡马斯兰染色观察到,此时 HUVEC 的核周出现许多小空泡样变性。2小时后,除培养液中6-酮-PGF_(1α)升高外,HUVEC 胞浆中 F-actin 含量也明显降低,扫描电镜可见 HUVEC 广泛收缩、部分细胞脱落、细胞间连接分离等现象。结论:HUVEC 在氧分压低于3.94kPa 时,对缺氧的耐受约1小时。2小时后,细胞广泛收缩,部分细胞脱落及微丝大量降解,HUVEC 发展成为不可逆性损伤。
Objective: To investigate the direct damage of vascular endothelial cells (VEC) induced by hypoxia and its influence. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in hypoxia environment with an oxygen partial pressure of 3.94kPa (1kPa = 7.5mmHg). The activities of lactate dehydrogenase (LDH) -PGF_ (1α) and intracellular polymerization of actin (F-actin) content and cell morphological changes. Results: Under hypoxic partial pressure for 1 hour, LDH activity in culture medium was significantly higher than that in control group. Camaraderne staining showed that there were many small vacuolated degeneration in the nucleus of HUVEC at this time. After 2 hours, except for the increase of 6-keto-PGF_ (1α) in culture medium, the content of F-actin in HUVEC cytoplasm also decreased obviously. Conclusion: HUVECs tolerate hypoxia for about 1 hour when oxygen partial pressure is lower than 3.94 kPa. After 2 hours, the cells were extensively contracted, part of the cells were shed, and the microfilaments were degraded in a large amount. HUVECs developed irreversible damage.