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蝙蝠葛碱(Dau)浓度依赖性抑制病人心房纤维及家兔房室结细胞APA,V_(max),减慢SR,病人心房纤维SP_4亦明显降低,并延长房室结细胞APD_(90)。利多卡因(Lid)在治疗浓度对AP各参数无明显影响,100μmol/L时明显降低病人心房纤维APA,V_(max),30μmol/L时降低兔房室结细胞V_(max)和SP_4。在两种标本,SR均呈减慢趋势。Dau明显延长家兔SACT,对SNRT,CSNRT,SNRTI和HR无明显影响,但与Lid合用可使CSNRT明显延长。提示Dau明显抑制窦房结传导功能,与Lid合用时使其自律性亦明显降低。Dau抑制心房纤维和房室结细胞AP可能为其临床上有效地治疗室上性快速型心律失常的主要电生理基础。
Dau concentration - dependently inhibited the APA, Vmax and SR of atrial fibrillation and atrioventricular node cells of rabbits in a concentration - dependent manner, but also significantly decreased the atrial fibers SP_4 and prolonged APD_ (90) in atrioventricular node cells. Lid at the therapeutic concentration had no significant effect on AP parameters. At 100μmol / L, the atrial fibrillation APA, Vmax and 30μmol / L decreased V_ (max) and SP_4 of rabbit atrioventricular node cells. In both specimens, SR showed a slowing trend. Dau significantly prolonged rabbit SACT, no significant effect on SNRT, CSNRT, SNRTI and HR, but in combination with Lid CSNRT can be significantly prolonged. Tip Dau significantly inhibit the conduction function of the sinus node, combined with Lid self-discipline is also significantly reduced. Inhibition of atrial fibrillation and atrioventricular node AP by Dau may be the primary electrophysiological basis for its clinically effective treatment of supraventricular tachyarrhythmia.