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.
出处
《中国药理学与毒理学杂志》
CSCD
北大核心
1995年第3期167-170,共4页
Chinese Journal of Pharmacology and Toxicology
关键词
吡那地尔
尼可地尔
来马卡林
血管平滑肌
缺氧
emakalim
pinacidil
RP 49356
nicorandil
cell hypoxia
lactate hydrogenase.malondialdehyde
muscle
smooth. Vascular