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作 者:杨梓琪[1] 程筠[1] 尚小珂[1] 钱成[1] 张光宇[1] 李行[1] 王扬淦[1]
机构地区:[1]武汉大学中南医院心内科,湖北武汉430071
出 处:《武汉大学学报(医学版)》2017年第4期544-548,共5页Medical Journal of Wuhan University
摘 要:目的:探讨正常、心衰时左心室内、外膜心肌细胞收缩舒张功能的差异。方法:采用主动脉缩窄术构建压力负荷型心衰小鼠。Langendorff灌流术分离小鼠左心室内、外膜心肌细胞。高速CCD摄像机系统和双激发荧光倍增系统同步测量内外膜心肌细胞肌小节收缩和胞内钙瞬变。张力传感器和微操作系统测量细胞的被动舒张张力(僵硬度)。结果:(1)正常小鼠内外膜收缩舒张功能存在差异,钙瞬变、钙Tau值、肌小节收缩幅度、僵硬度均为内膜大于外膜;(2)心衰时,小鼠左心室内外膜收缩舒张功能都受损,钙瞬变内外膜均降低,肌小节收缩幅度均减小,僵硬度均增大;(3)心衰时内外膜的钙瞬变差异消失,而肌小节收缩和僵硬度的差异依然存在。结论:正常心脏内膜是产生心肌收缩力的主要力量,心衰时内外膜细胞收缩舒张功能均受损,且内外膜本来存在的部分梯度差异在心衰时消失。Objective: To evaluate the transmural heterogeneity in left ventricular in normal and heart failure(HF) mice. Methods: Severe thoracic aortic banding was adopted to accquire pressure overloaded HF mouce model. Endocardial(Endo) and epicardial(Epi) myocytes were isolated from C57/BL6 mice by Langendorff perfusion system. Sarcomere length and calcium transient were recorded by Ionoptix dual excitation fluorescence photomultiplier system. A tension sensor was used to get the cell's stiffness. Results: ① Endo and Epi cells of normal mice have different features in sarcomere contraction, calcium transient, and stiffness, as the calcium transient in endo (0. 295-0. 019)F340/380 (n= 21) is greater than that in epi (0. 254±0. 013)Fa40/3s0 (n = 19, P〈 0.05) ; ②When heart failure, both the endo and epi cells become worse in systolic and diastolic function; ③The transmural heterogeneity in normal heart disappeared in HF heart, the calcium transient in endo cells (0. 197±0. 015)F340/380 (n= 16)have no significant difference from that in epi cells (0. 191±0. 024)F340/380 (n= 15). Conclusion: Endo cells play a key role in heart contraction; Both endo and epi cells get impaired when heart failure; Part of the transmural heterogeneity features disappear when heart failure.
关 键 词:心衰 内外膜 心肌细胞收缩 钙瞬变 被动舒张张力
分 类 号:R541.6[医药卫生—心血管疾病]
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