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机构地区:[1]贵州省人民医院心外科,贵州贵阳550002 [2]华中科技大学同济医学院附属协和医院心外科,湖北武汉430022 [3]贵州省人民医院肿瘤科,贵州贵阳550002
出 处:《中国现代医学杂志》2015年第19期17-20,共4页China Journal of Modern Medicine
基 金:贵州省科技计划(No:黔科合LS[2011]040号)
摘 要:目的通过全细胞膜片钳技术研究蛋白激酶C(PKC)激动剂豆蔻酰佛波醇乙酯(PMA)对人心房肌细胞肿胀激活的氯离子电流(ICl.swell)的作用。方法术中取患者右心房组织,酶解分离出心房肌细胞。全细胞膜片钳技术记录氯离子电流。低渗台氏液灌流激活胞肿胀激活的氯离子电流后再加入PMA,观察电流变化。结果胞肿胀激活的氯离子电流达到稳定状态后再用含有1μmol/L PMA的低渗台氏液灌流,从-110 m V到+60 m V,除了在-10 m V,电流密度均增加(P<0.05,n=7)。该效应在洗脱后或者加入氯离子电流阻断剂二异氰酸二磺酸后减弱。结论该研究通过全细胞膜片钳技术观察到蛋白激酶C激动剂PMA可以增强人心房肌细胞ICl.swell。但对其机制,还需要进一步研究。[Objective] To study the function of phorbol-12-myristate-13-acetate (PMA), a protein kinase C (PKC) agortist, in the regulation of swelling-activated chloride currents (ICl.swell) in human atrial myocytes via the whole-cell patch-clamp technique. [Methods] Human right atria/appendages were obtained from patients undergo- ing cardiosurgery. Single human atrial myocytes were dispersed enzymatically. ICl.swell was evoked under hypotonic solution and recorded via the whole-cell patch-clamp technique, either in the presence or absence of PMA. [ Re- suits ] After ICl.swell approached steady state, subsequent exposure to 1 μmol/L PMA caused substantial augment of current density in the whole range of voltage (from -110 mV to +60 mV) except in -10 mV (P 〈 0.05, n = 7). The effect attenuated after washout or the addition of chloride current inhibitor, 4,4-diisothiocyanostilbene -2,2-disulfon- ic acid. [ Conclusions ] By using the whole-cell patch-clamp technique, PMA, a PKC agonist, was found to enhance ICl.swell in human atrial myocytes, and the underlying mechanism needs further study.
关 键 词:肿胀激活的氯离子电流 豆蔻酰佛波醇乙酯/PMA 蛋白激酶C 人类 心房肌细胞
分 类 号:Q331[生物学—遗传学] R541[医药卫生—心血管疾病]
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