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作 者:李翔[1] 张季谦[1,2] 程睿[1] 蒋迎芳[1] 高飞[1]
机构地区:[1]安徽师范大学物理与电子信息学院,芜湖241000 [2]曼彻斯特大学物理与天文系生物物理中心
出 处:《生物医学工程学杂志》2013年第4期697-703,共7页Journal of Biomedical Engineering
基 金:国家自然科研基金资助项目(11047017);安徽省自然科研基金资助项目(2009KJ099B)
摘 要:目前对于SCN5A基因突变导致窦房结(SAN)起搏功能异常的有效治疗仍在探索之中。本文以二维兔子SAN-心房细胞实验解剖模型为基础,考虑基因突变的存在,合理引入体系的酸浓度和温度的影响,研究了体系酸浓度及温度对病态窦房结综合征(SSS)的调节作用。结果表明:位于SCN5A基因上的两个位点(T220I和delF1617)的异常使得Na+电流减少,导致SAN的起搏功能异常;适当调节体系的酸浓度及温度,一方面可使得相应膜电流增加,另一方面也可增大因突变而减小的Na+电流,从而使SAN组织异常的搏动恢复到正常状态。模拟结果表明SAN体系的异常搏动机制与离子通道间的SCN5A基因突变密切相关,而体系的酸浓度与温度则有一定的调节作用,该模拟结果可为临床上医学诊断和治疗提供一定的理论依据。The effective therapeutics for the sinoatrial node (SAN) pacemaker dysfunction induced by SCN5A gene mutation this is still being explored recently. In this study, a two-dimensional experimental model of rabbit SAN-atrial cell system which proposed by Zhang et al. , was used as a prototype, the gene mutation was considered, and effects of both the acid concentration and temperature were also introduced. The effects of acid concentration and temperature on sick sinus syndrome (SSS) at the tissue level were investigated by simulation. The results showed that the SAN abnormal pacemaker could be caused by the reduction of INa, which is induced by the two mutations of T220I and delF1617. The results also showed that if we properly adjusted the acid concentration and temperature of the system, not only could we increase the relevant currents, but also could we increase INa which reduced by gene mutations, so that the pacemaking behavior of SAN tissue could return to normal state from abnormalities. The above simulation results imply that the abnormal pacemaking of SAN system may closely relate to the gene mutation of ion channel mutations, and the acid concentration and temperature may play a modulatory role. Our study could be useful for clinical medical diagnosis and therapy of cardiac disease.
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