摘要
目的 :观察比索洛尔对培养的人脐静脉内皮细胞 (HU VECs)在缺氧 /复氧 (A/ R)过程中一氧化氮 (NO)生成的影响。方法 :将 HUVECs暴露于缺氧环境中 30 m in后复氧 ,并加入比索洛尔 (1,5 0和 5 0 0 μmol/ L)或空白对照 ,测量复氧前、复氧后 1和 4h培养液上清 NO含量。结果 :对照组 NO产量在复氧后 1h,4h与复氧前相比有显著下降 (均 P<0 .0 1)。比索洛尔 5 0 μm ol/ L 组和 5 0 0 μmol/ L 组 NO产量在复氧后 1h,4h与复氧前相比无显著差异 (均P>0 .0 5 ) ,而与对照组和 1μmol/ L 组同一时间相比均有显著增加 (均 P<0 .0 1)。结论 :比索洛尔可以阻止 A/ R期间内皮细胞 NO产量的下降 ,因此 NO可能参与了 β阻滞剂减少缺血再灌注损伤的过程。
AIM: To investigate the effects of bisoprolol on nitric oxide (NO) production by cultured human umbilical vein endothelium cells(HUVECs) during anoxia/reoxygenation(A/R). METHODS:After 30 min period of anoxia by exposing HUVECs monolayers to a chamber filled with 100% N 2,reoxygenation was initiated, and meanwhile Bisoprolol (1,50,500 μmol/L or control) was added to HUVECs monolayers. Products of NO in HUVECs supernatants were determined 0,1 and 4h after reoxygenation. RESULTS:In control group, level of products of NO decreased significantly 1 h ( P <0.01) and 4 h ( P <0.01) after reoxygenation. Adding of 50 μmol/L or 500 μmol/L Bisoprolol resulted in maintaining of NO products ( P >0.05),and comparing to control and 1 μmol/L Bisoprolol group level of products of NO increased significantly in 50 μmol/L and 500 μmol/L Bisoprolol group 1, 4 h after reoxygenation ( P <0.01). CONCLUSION:Bisoprolol can prevent level of endothelium derived NO from decreasing during A/R, so NO may play a role in the mechanism by which β blockers can reduce ishemic reperfusion injury.
出处
《心脏杂志》
CAS
2001年第2期93-94,97,共3页
Chinese Heart Journal
关键词
比索洛尔
缺氧
复氧
内皮
一氧化氮
bisoprolol
anoxia/reoxygenation
endothelium
nitric oxide
