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作 者:欧阳平[1] 邓春玉[2] 刘文华[3] 王磊[3] 梁东[3] 钱卫民[2] 徐安龙[3]
机构地区:[1]第一军医大学南方医院心血管内科,广东广州510515 [2]广东省人民医院电生理研究室,广东广州510080 [3]中山大学生命科学学院国家高技术发展计划海洋功能基因组开放实验室,广东广州510275
出 处:《第一军医大学学报》2004年第6期609-613,618,共6页Journal of First Military Medical University
基 金:This study is supported by State Hi-Tech Development Project of China (2001AA628090) ;by Guangzhou Sci-tech Committee Foundation (2002Z3-E4131)
摘 要:目的观察新型基因重组海葵毒素rhk2a对大鼠心室肌细胞离子通道的影响。方法采用全细胞膜片钳技术分别记录rhk2a对大鼠心室肌细胞钠电流、L型钙电流和钠-钙交换电流的影响。结果与对照组相比,新型重组海葵毒素rhk2a能够明显减慢大鼠心室肌细胞钠通道的时间依赖性失活(τh)(14.15±4.6 ms vs2.03±0.30 ms, P<0.05),而rhk2a对大鼠心室肌细胞钙通道电流(-8.86±0.35 PA/PF vs-8.99±0.64 PA/PF,P>0.05)和钠-钙交换电流(-0.65±0.2 PA/PF vs-0.69±0.15 PA/PF, P>0.05)无明显直接作用。结论rhk2a对大鼠心室肌细胞钠通道的时间依赖性失活的减慢是rhk2a对心脏具有正性肌力效应的重要机制。Objective To determine the ionic mechanisms of a novel neurotoxin rhk2a obtained from the sea anemone Anthopleura sp.in rat ventricular myocytes. Methods Whole-cell patch-clamp recording technique was used to record the sodium, calcium, and sodium-calcium exchange currents (I Na , I Ca, L and I Na-Ca , respectively) in the isolated single rat ventricular myocytes with or without rhk2a treatment. Results The current-voltage (I-V) relationship for whole-cell I Na in the non-treated and rhk2a-treated (at the dose of 1 μmol/L) myocytes showed no significant difference (P>0.05), but the time constants for inactivation (τ h ) were significantly greater (P<0.05) for the treated cells over the entire course of the experiment, while the time constants for activation (τ m ) exhibited no significant difference between the two cells. The inactivation curve of I Na of rhk2a-treated cells was similar to that of the non-treated cells, as with the I-V relationship for whole-cell L-type calcium current (I Ca,L ) and I Na-Ca ). Conclusions Delayed inactivation of Na + channel plays an important role in the positive inotropic effect of rhk2a, possibly resulting from the alteration in Na + channel kinetics induced by rhk2a. rhk2a does not directly affect I Ca, L or I Na-Ca .
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