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机构地区:[1]第三军医大学西南医院心血管内科,重庆市介入心脏病学研究所,重庆400038
出 处:《第三军医大学学报》2006年第4期305-307,共3页Journal of Third Military Medical University
基 金:国家自然科学基金资助项目(30070314)~~
摘 要:目的通过比较模拟缺血预适应(IP)及模拟/再灌注(I/R)对原代培养乳鼠窦房结细胞起搏离子流(IF)的影响,探讨IP对I/R时乳鼠窦房结细胞电生理活动的保护作用。方法取培养2D的乳鼠窦房结细胞,随机分为①对照组;②模拟I/R组;③模拟IP组。以全细胞膜片钳技术检测窦房结细胞IF的变化。结果①模拟I/R组各指令电压下的IF密度较对照组显著增高,激活曲线右移,半数最大激活电压由(-98.9±2.4)MV变为(-85.2±2.5)MV(P<0.01)。②模拟IP能显著降低I/R后的IF密度,使激活曲线左移,半数最大激活电压变为(-93.3±2.8)MV(P<0.01),但未恢复到对照水平(P<0.05)。结论模拟IP可抑制模拟I/R后活化增强的IF,有助于维护I/R时窦房结细胞电生理活动的相对稳定性。Objective To compare the effects of stimulated ischemic preconditioning (IP) and ischemia/ reperfusion (I/R) on the hyperpolarization-activated current (If) of sinoatrial node cells and explore the mechanisms of electrophysiological protection of IP. Methods The sinoatrial node cells cultured for 2 d were randomized to three groups: ① Control in which the cells were cultured at 37 ℃ in the mimic reperfusion solution, meanwhile the mixture of 95% O2 and 5% N2 was ventilated; ② I/R in which the cells were cultured in the mimic ischemic solution and simultaneously the mixture of 95% 02 and 5% N2 was ventilated for 3 h, then cultured in the mimic reperfusion solution and simultaneously the mixture of 95% O2 and 5% N2 was ventilated for 4 h;③ IP in which the cells underwent ischemia for 10 min and reperfusion for 10 min, repeated once. Then the cells were treated as the same as the I/R group. After 4-hour reperfusion, If was recorded by wholecell patch clamp technology. Results I/R significantly enhanced the current density of If, shifted the current activation curve to more positive value by changing the half-activation voltage from ( - 98.9± 2.4 ) mV to ( -85.2 ±2.5)mV (P 〈 0. 01 ). Although not recovered to the normal level, IP reduced the current density of If raised by I/R, shifted the current activation curve to more negative value and changed the half-activation voltage to ( - 93.3 ± 2.8) mV (P 〈 0. 01 ). Conclusion IP makes current density and kinetics of If approach the normal level, and participates in maintaining electrophysiological stability of sinoatrial node cells during I/R.
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