三丙酮胺对心肌细胞膜电位的影响 Ⅱ.抗心肌缺血缺氧的电生理学研究

Effects of Triacetonamine-HCL(TAA) on Myocardial Transmembrane Potentials——Ⅱ. The Electrophysiological Study of Anti-myocardial Hypoxia and Ischemia of Triacetonamine

本文用电生理学实验证明:三丙酮胺(TAA)有效地改善缺氧台氏(Tyrode)液灌流所致的心肌电活动异常;明显减轻关闭呼吸机致整体动物心肌缺氧时动作电位变态的程度;显著抵抗静脉注射垂体后叶素诱发在位心脏急性心肌梗塞的电生理异常反应。

Triacetonamine-HCI(TAA) is synthesized artificially based on the molecularstructure of the substance isolated from South China sea Juncella squamata. Theelectrophysiological study of anti-myocardial hypoxia and ischemia of TAA wascarried out.60 min after superfusion with O_2-free Tyrode solution, APA, Vmax,RP, APD and ERP were all reduced and the pIateau disappeared. If TAA(5mM)was added at this time, all of the parameters of action potential retained to normal.1f TAA was added before O_2free, the appearence of abnormal action potentialswas greatly delayed. By pretreatment with TAA(5mg/kg, iv), the hypoxia-likeaction potentials were significantly allevieted in guinea pigs in vivo. The resultsshow that TAA has an anti-myocardial hypoxia effect. The ischemia-like actionpotentials were observed by iv pituitrin 0.3ug/kg on guinea pigs in vivo, butwere'nt after pretreatment with iv TAA 5mg/kg. The result shows that TAAhas an anti-myocardial ischemia effect. All of the effects of TAA were reversible.