摘要
用标准微电极技术研究胍丁胺对异丙肾上腺素 ( Iso)诱发人心房纤维迟后除极的影响 .结果如下 :( 1 )胍丁胺 ( 1 - 1 0 mmol· L-1)以浓度依赖地方式明显抑制 Iso( 2 0 nmol· L-1)诱发人心房纤维的迟后除极 ;( 2 )预先应用咪唑啉受体和 α2 肾上腺素受体拮抗剂咪唑克生 ( 0 .1 mmol· L-1)可阻断胍丁胺 ( 1 0 mmol· L-1)对 Iso( 2 0 nmol· L-1)诱发迟后除极的抑制作用 ;( 3)预先应用一氧化氮合酶抑制剂硝基 - L-精氨酸甲酯 ( 0 .5mmol· L-1) ,不影响胍丁胺 ( 1 0 mmol· L-1)对 Iso( 2 0 nmol· L-1)诱发迟后除极的抑制作用 .结果表明 ,胍丁胺对 Iso诱发人心房纤维迟后除极的抑制作用可能是由于咪唑啉受体和 α2 肾上腺素受体介导钙内流减少所致 .
The effects of agmatine on delayed afterdepolarizations (DAD) induced by isoprenaline (Iso) were studied in human atrial fibers obtained at cardiac surgery using standard microelectrode techniques. The results obtained are as follows. (1) DAD induced by Iso (20 nmol·L -1 ) were markedly inhibited by pretreatment with agmatine (1-10 mmol·L -1 ) in a concentration dependent manner. (2) The inhibitory effects of agmatine (10 mmol·L -1 ) on DAD induced by Iso (20 nmol·L -1 ) were reversed by pretreatment with idazoxan (0.1 mmol·L -1 ), an alpha 2 adrenergic receptor (α 2 AR) and imidazoline receptor (IR) antagonist. (3) N G nitro L arginine methyl ester (0.5 mmol·L -1 ), a NO synthase inhibitor, did not affect the inhibitory effects of agmatine (10 mmol·L -1 ) on DAD induced by Iso (20 nmol·L -1 ). The results indicate that the inhibitory effects of agmatine on DAD induced by Iso in human atrial fibers may be due to a decrease in calcium influx which mediated by IR and α 2 AR.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2000年第4期247-252,共6页
Chinese Journal of Pharmacology and Toxicology
关键词
胍丁胺
异丙肾上腺素
微电极
心房纤维迟后除极
agmatine
heart atrium
isoprenaline
idazoxan
microelectrodes
action potentials