IHC-66对豚鼠心室乳头状肌细胞缺氧与再给氧后跨膜电活动的影响

目的观察IHC-66对缺氧与再给氧后，豚鼠心室乳头状肌细胞电活动的影响，探讨其抗心律失常的机制。方法采用常规玻璃微电极技术，以离休豚鼠心室乳头肌为标本，研究IHC-66对豚鼠心室乳头肌细胞动作电位各参数的影响。结果IHC-66（10～30μmol·L-1）可呈现出浓度依赖性的对抗缺氧引起的动作电位时程（APD）的缩短。此外，IHC-66（10μmol·L-1）还可部分拮抗吡那地尔（pinacidil50μmol·L-1）缩短APD的作用，并可部分减少缺氧造成的豚鼠心室乳头状肌细胞组织中ATP水平的下降。结论IHC-66对缺氧与再给氧后豚鼠心室乳头状肌细胞电活动的影响，可能与其对K+-ATP通道的阻滞并部分减少心肌细胞ATP的消耗有关。

IHC-66 on the transmembrane action potentials of guinea pig papillary muscles during hypoxia and reoxygenation

AIM To determine whether IHC-66 [3, 6-di (dimethylamino )-dibenzopyriodonium of ferric EDTA] may exert beneficial effects on the transmembrane action potentials during hypoxia and reoxygenation in isolated right ventricular papillary muscles of the guinea pig. METHODS The effects of IHC-66 on transmembrane action potentials of guinea pig papillary muscles during hypoxia and reoxygenation were studied using conventional microelectrode techniques. Right ventricular papillary muscles of the guinea pig in which ATP level was also determined by the luciferase method. RESULTS Hypoxia conditions induced a decrease in action potential duration (APD) without significantly affecting other action potential parameters. IHC-66 inhibited this hypoxia-induced decrease in APD. Pinacidil-induced shortening of APD was antagonized by IHC-66. Hypoxia significantly decreased the myocardial adenosine triphosphate (ATP) level, which was also prevented partly by IHC-66. CONCLUSION These results suggested that IHC-66 may inhibit the hypoxia induced shortening of APD by some mechanism, which contribute to the blocking K+-ATP channels and decrease in Ca2+、 Na+ inward current.