摘要
目的：研究凝血酶受体激活肽（TRAP）对豚鼠心室肌细胞腺嘌呤核苷三磷酸（ATP）敏感性钾（K。）通道的作用及在保护心肌细胞方面的作用。方法：对健康成年豚鼠采取心室肌细胞急性分离，采用单通道膜片钳记录技术中的细胞贴附式及内面向外模式记录吡那地尔（Pinacidil）、ATP、格列苯脲（Glibenclamide）、TRAP对豚鼠单个心室肌细胞K。通道电流的影响。结果：加入吡那地尔后Km通道的通道活动度（0．55±0．07）比加药之前（0．23±0．05）±曾加（记录5次）；在吡那地尔存在时，加入ATP后KATP通道的通道活动度（0．67±0．14）较加入ATP之前（0．10±0．05）减少（记录4次）；加入格列苯脲后K椰通道的通道活动度（0．56±0．12）比加药前（0．06±0．03减少（记录5次）；加入TRAP后通道的通道活动度（0．48±0．11）比加入TRAP前（0．15±0．11）增加（记录5次），上述比较差异均有统计学意义（P〈0．05～0．01）。结论：TRAP激活心室肌细胞K。通道，对心肌细胞具有保护作用。
Objective： To investigate the effect of thrombin receptor activator peptide （TRAP） on KATP channel of ventricular myocyte, and to identify the protective roll of the KATP channel for the myocardial cells in experimental guinea pigs. Methods： Swiftly separated guinea pig single myocardial cell was treated with pinacidil, glibenclamide and TRAP respectively, the KATP channel opening probability （NPo） changes were detected by the single-channel patch-clamp technique in different groups. Results： ① For pinacidil treated cells, the KATP NPo increased than it was before the treatment, （0.55 ± 0.07） vs （0.23 ± 0.05）, n=5 records and with pinacidil existing, the KATP NPo decreased by ATP addition, （0.67 ± 0.14） vs （0.10 ±0.05）, n=4 records. ② For glibenclamide treated cells, the KATv NPo decrease than it was before （0.56 ± 0.12） vs （0.06±0.03）, n=5 records. ④ For TRAP treated cells, the KATP NPo increased than it was before, （0.15± 0.11） vs （0.48 ± 0.11）, n=5 records. All the above changes had the statistic meaning, all P〈0.05-0.01. Conclusion： TRAP may activate the KATP channel of ventricular myocyte and protect myocardial cell in experimental guinea pigs.
出处
《中国循环杂志》
CSCD
北大核心
2013年第7期537-541,共5页
Chinese Circulation Journal
