吡那地尔，尼可地尔，来马卡林和RP49356对血管平滑肌细胞缺氧损伤的保护作用  

Protective effects of pinacidil, nicorandil, lemakalim andRP 49356 on hypoxia of vascular smooth muscle cells 1

作　　者：史道华[1] 郭兆贵[1] 

机构地区：[1]湖南医科大学药理学研究室

出　　处：《中国药理学与毒理学杂志》1995年第3期167-170,共4页Chinese Journal of Pharmacology and Toxicology

摘　　要：来马卡林，吡那地尔，尼可地尔及ＲＰ４９３５６对培养的兔胸主动脉平滑肌细胞缺氧（ＮａＣＮ，２ｍｍｏｌ·Ｌ－１）１．５ｈ及４ｈ引起的乳酸脱氢酶释放呈剂量依赖性抑制；尼可地尔及ＲＰ４９３５６组预先给予格列本脲（１μｍｏｌ·Ｌ－１），其抑制作用明显减弱，四药降低缺氧４ｈ时细胞丙二醛产量亦呈剂量依赖性；ＲＰ４９３５６组预先加入格列本脉，此种作用被显著抑制，结果提示，四药对血管平滑肌细胞缺氧所致的损害具有保护作用。The protective effects of potassium channelopeners (KCOs) lemakalim, pinacidil. nicorandil and RP49356 on vascular smooth muscle cells (VSMC) againsthypoxia were tested. Hypoxia model was made by addedNaCN (2 mmol . L-1) into VSMC (10 5 well1) to induceATP depletion. Pretreated with the four KCOs beforehypoxia 30 min, lactate dehydrogenase release from VSMCwere significantly inhibited in a dosedependent rnanner af-ter period of 1.5 h and 4 h hypoxia, respectively. The effectof the four agents (10 μmol. L-1) was blockcd byglibenclamide (l pmol . L'). In addition. malondialdehydeproduction of VSMC was markedly decreased by the fourKCOs in a dosedependent manner afler period of 4 hhypoxia. In RP 49356 flo pmol . L-1) group, the effect ofRP 49356 on malondialdehyde production was significantlyinhibited by glibenclamide (0. 14 ± 0. 1 5 vs 1 .59 ± 0.36 μmol ·well-1, P<0.001). These results demonstrated that the fourKCOs prevented VSMC injury from hypoxia by decreasinglipid superoxidation via hyperpolarizing cell rnembrane.

关 键 词：吡那地尔 尼可地尔 来马卡林 血管平滑肌 缺氧 

分 类 号：R543[医药卫生—心血管疾病] R972[医药卫生—内科学]