摘要
用新生大鼠心肌细胞制备缺氧缺糖模型，取其培养液测定ＬＤＨ释放量。结果显示，在加入血小板活化因子（ＰＡＦ）后，缺气缺糖的心肌细胞ＬＤＨ峰放量显著增加。ＰＡＦ拮抗剂ＢＮ５０７３０（ＢＮ５０７３０），钙拮抗剂维拉帕米和比帕里定均能显著抑制因ＰＡＦ所致缺氧缺糖心肌细胞释放ＬＤＨ。提示ＰＡＦ可加重缺氧缺糖心肌细胞的损伤，ＰＡＦ拮抗剂和钙拮抗剂均对ＰＡＦ加重缺氧缺糖心肌细胞损伤具有保护作用。
he effect of platelet
activating factor(PAF)during the acute anoxia phase of myocytescultured from neonatal rats
was studied.Lactate dehydrogenase(LDH) in culture mediumwas determined as an index for
cellular damage. The results showed that PAF significantlyincreased LDH release of anoxia
myocytes in a dose-dependent manner but without signifi-cant effect on that of normoxia
myocytes. PAF antagonist BN50730,calcium antagonists(ver-apamill and bepridil)significantly
decreased LDH release of PAF-treated anoxic myocytes.Itis sugggested that PAF antagonist
and callcium antagonist alleviate the cellular damage in-duced by PAF.
出处
《湖南医科大学学报》
CSCD
1994年第4期283-286,共4页
Bulletin of Hunan Medical University
关键词
血小板活化因子
心肌细胞损伤
PAF拮抗剂
钙拮抗
platelet
activating factor
myocardium
cells, cultured
anoxia
PAFantagonist
calcium channel
blockers
drug effect
rats
