摘要
目的 :探讨低氧引起冠状动脉内皮细胞 (CAEC)释放ET - 1、NO和PGI2 改变的机制。方法 :运用放射性 [45Ca2 + ]掺入、放免和比色等方法 ,测定常氧组、低氧组冠状动脉内皮细胞钙摄取率 ,以及常氧组、低氧组、低氧 +维拉帕米组冠状动脉内皮细胞培养液中ET - 1、NO和PGI2 含量。结果 :低氧组CAEC [45Ca2 + ]摄取率为 (2 9 6± 3 7)ng/gprotein/ 30min ,常氧对照组为 (15 2± 1 1)ng/gprotein(P <0 0 1)。低氧 +维拉帕米组ET - 1分泌量显著多于低氧组 (P <0 0 1)。低氧 +维拉帕米组分泌的NO显著低于低氧组 (P <0 0 5 ) ,与常氧组相差不显著。低氧 +维拉帕米组分泌的PGI2 显著多于低氧组 ,与常氧组相差不显著。结论 :低氧时引起的NO、ET - 1、PGI2 分泌改变与低氧引起的冠状动脉内皮细胞Ca2 + 内流增加有关。
AIM: To explore the mechanism of ET-1, NO and PGI 2 release from coronary artery endothelial cells (CAEC) induced by acute hypoxia. METHODS: Bovine coronary artery endothelial cells were cultured and [ 45 Ca 2+ ] was used to investigate the difference of calcium uptake between normoxia group and hypoxia group (3% O 2). The contents of ET-1, NO and PGI 2 in media of normoxia group, hypoxia group and hypoxia + verapamil group were measured 24 h after hypoxia. RESULTS: [ 45 Ca 2+ ] uptake by CAEC in hypoxia group was 1.9 times more than normoxia group ( P< 0 01). Hypoxia + verapamil group released more PGI 2, ET-1 and less NO than hypoxia group ( P< 0 05). CONCLUSION: Changes of ET-1, NO and PGI 2 releases during hypoxia may be caused by the inflow of Ca 2+ into coronary artery endothelial cells.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第9期1109-1111,共3页
Chinese Journal of Pathophysiology