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作 者:王宪沛[1] 马季骅[1] 张培华[1] 李俊[1]
机构地区:[1]武汉科技大学医学院心脏电生理研究室,湖北武汉430080
出 处:《中国应用生理学杂志》2006年第1期16-20,共5页Chinese Journal of Applied Physiology
基 金:湖北省自然科学基金项目(2003ABA189);湖北省教育厅科学基金项目(2002AB1101)
摘 要:目的:研究心室肌细胞持续性钠电流(INa.P)在缺氧/复氧早期的变化,探讨其在此病理条件下的作用及意义。方法:运用全细胞膜片钳技术记录持续性钠电流,并观察其在缺氧-复氧模型下的变化。结果:①在0.5Hz,1Hz和2Hz的刺激频率下第1个和第8个刺激脉冲引起的INa.P电流密度差值分别为(0.021±0.014)pA/pF,(0.097±0.014)pA/pF和(0.133±0.024)pA/pF(P<0.01);②分别在-150^-80mV,阶跃10mV的钳制膜电位下去极化至-30mV,INa.P逐渐减小;③在缺氧条件下,INa.P电流密度增大,并随缺氧时间延长增大更显著;④在正常、缺氧15min和复氧5min时INa.P密度分别为(0.500±0.125)pA/pF,(1.294±0.321)pA/pF和(0.988±0.189)pA/pF(与对照比较P<0.01)。结论:以上特性提示INa.P在缺氧/复氧过程心律失常的产生及钙超载引起心肌损伤的机制中起重要作用。Aim: To investigate the effect of hypoxia/early reoxygenation on persistent sodium current( INa.p) in single ventricular myocytes of guinea pig and discuss its role and significance during this pathological condition. Methods: The whole cell patch clamp technology was used to record this current and study its change under the condition of hypoxia/reoxygenation model. Results- OWith 0.5 Hz, 1 Hz and 2 Hz pulse frequency, the current density gap between the first and the eighth pulse of INa. p was (0. 021±0. 014)pA/ pF, (0. 097 ± 0. 014)pA/pF and (0. 133 ±0. 024)pA/pF( P〈 0.01 )respectively. ②Depolarization with membrane holding potential of - 150~ -80 mV respectively, INa.p density attenuated gradually. ③The amplitude of INa.p was increased consistently with the prolongation of hypoxia time during hypoxia. ④INa.p was (0. 500 ± 0. 125)pA/pF, (1. 294 ± 0. 321) pA/pF and (0. 988 ± 0. 189) pA/pF( P〈 0.01, vs normoxia, respectively)during normoxia, hypoxia after 15 min and reoxygenation after 5 min, respectively. Conclusion: These results indicate that INa. p has great significance in arrhythmogenesis and calcium-overload, which causes the following postischemia and posthypoxia myocardial damage.
分 类 号:R331.3[医药卫生—人体生理学]
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