肿瘤坏死因子α抑制豚鼠急性缺血心室肌细胞L型钙通道电流  

Inhibition of Tumor Necrosis Factor-aon L-type Calcium Current in Guinea Pig Ventricu- lar Myocytes accmpany simulation of Acute Ischemia

作　　者：吴黎明[1] 唐闽[1] 

机构地区：[1]福建医科大学附属协和医院急诊科福建省冠心病研究所,福建省福州市350001

出　　处：《中国动脉硬化杂志》2004年第3期287-290,共4页Chinese Journal of Arteriosclerosis

基　　金：福建省医学创新课题项目(2003-CX-18)资助

摘　　要：为探讨肿瘤坏死因子α对正常及模拟缺血状态下豚鼠心室肌细胞L型钙通道电流的影响。全细胞膜片技术记录豚鼠心室肌细胞单个L型钙通道电流。肿瘤坏死因子α(100、300和500 ku/L)对豚鼠心室肌细胞L型钙通道电流峰值的影响与对照组均无明显差异(P>0.05),但模拟急性缺血时,同浓度的肿瘤坏死因子α却明显抑制豚鼠心室肌细胞L型钙通道电流峰值并呈浓度依赖性,抑制率分别为46.5％±3.5％、62.7％±3.0％和80,7％±3.7％,与对照组和单纯缺血组相比差异明显(均P<0.05)。正常灌流液中不同浓度的肿瘤坏死因子α对豚鼠心室肌细胞峰值L型钙通道电流无明显影响;但模拟急性缺血时其却呈浓度依赖性地增强缺血对豚鼠心室肌细胞的L型钙通道电流峰值抑制作用。Aim To study the effect of TNFαon L-type cacium channel current (ICa-L) in isolated guinea pig ventricular myocytes in normal Tyrode solution and with imitating acute ischemia. Methods Using the whole cell patch clamp technique in isolated guonea pig ventricular myocates both normal Tyrode solution or simulation of acute ischemia. Results Under normal Tyrode solution, the application of TNFα (100 kU/L, 300 kU/L and 500 kU/L) did not produce any detectable alterations on peak of ICa-L, but inhibitory rate on peaks of ICa-L were decreased markedly by 46.5% ± 3.5% , 62.7%±3.0% and 80.7% ±3.7% respectivelyby TNFα at the same concentration accompany simulation of acute ischemia and showed dose-dependence; there are significant difference compare with control group or simulate of acute ischemia alone group ( P < 0.05, respectivelyby) . Conclusion TNFαrwould not alter peak of ICa-L in guinea pig ventricular cells under normal Tyrode solution; but increased inhibitory effects of ischemia on peaks of ICa-L accompany imitation of acute ischemia and showed concentration-dependence .

关 键 词：生理学 肿瘤坏死因子α抑制钙通道电流 膜片钳技术 心室肌细胞 豚鼠 CA^2+通道 L型 

分 类 号：R33[医药卫生—人体生理学]