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神经生长因子对兔心肌梗死后动作电位时程及复极电流的影响。

Effects of nerve growth factor on the action potential duration and repolarizing currents in a rabbit model of myocardial infarction.

机构信息

Institute of Geriatric Cardiology of Chinese PLA General Hospital, 28 Fuxing Road, 100853 Beijing, China.

出版信息

J Geriatr Cardiol. 2013 Mar;10(1):39-51. doi: 10.3969/j.issn.1671-5411.2013.01.008.

DOI:10.3969/j.issn.1671-5411.2013.01.008
PMID:23610573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3627714/
Abstract

OBJECTIVES

To investigate the effect of nerve growth factor (NGF) on the action potential and potassium currents of non-infarcted myocardium in the myocardial infarcted rabbit model.

METHODS

Rabbits with occlusion of the left anterior descending coronary artery were prepared and allowed to recover for eight weeks (healed myocardial infarction, HMI). During ligation surgery of the left coronary artery, a polyethylene tube was placed near the left stellate ganglion in the subcutis of the neck for the purpose of administering NGF 400 U/d for eight weeks (HMI + NGF group). Cardiomyocytes were isolated from regions of the non-infarcted left ventricular wall and the action potentials and ion currents in these cells were recorded using whole-cell patch clamps.

RESULTS

Compared with HMI and control cardiomyocytes, significant prolongation of APD50 or APD90 (Action potential duration (APD) measured at 50% and 90% of repolarization) in HMI + NGF cardiomyocytes was found. The results showed that the 4-aminopyridine sensitive transient outward potassium current (I to), the rapidly activated omponent of delayed rectifier potassium current (I Kr), the slowly activated component of delayed rectifier potassium current (I Ks), and the L-type calcium current (I CaL) were significantly altered in NGF + HMI cardiomyocytes compared with HMI and control cells.

CONCLUSIONS

Our results suggest that NGF treatment significantly prolongs APD in HMI cardiomyocytes and that a decrease in outward potassium currents and an increase of inward Ca(2+) current are likely the underlying mechanism of action.

摘要

目的

研究神经生长因子（NGF）对兔心肌梗死模型中未梗死心肌动作电位和钾电流的影响。

方法

制备左前降支冠状动脉闭塞的兔模型，允许其恢复 8 周（愈合性心肌梗死，HMI）。在左冠状动脉结扎手术中，在颈部皮下靠近左星状神经节放置聚乙烯管，目的是给予 NGF 400 U/d 共 8 周（HMI + NGF 组）。从非梗死左心室壁区域分离心肌细胞，并使用全细胞膜片钳记录这些细胞中的动作电位和离子电流。

结果

与 HMI 和对照心肌细胞相比，HMI + NGF 心肌细胞中的 APD50 或 APD90（复极化 50%和 90%时的动作电位时程（APD））明显延长。结果表明，4-氨基吡啶敏感的瞬时外向钾电流（Ito）、快速激活延迟整流钾电流的组成部分（I Kr）、缓慢激活延迟整流钾电流的组成部分（I Ks）和 L-型钙电流（I CaL）在 NGF + HMI 心肌细胞中与 HMI 和对照细胞相比均发生了显著改变。

结论

我们的结果表明，NGF 治疗可显著延长 HMI 心肌细胞的 APD，外向钾电流减少和内向 Ca（2+）电流增加可能是其作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/4612e501d4bf/jgc-10-01-039-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/0ab94a198a0d/jgc-10-01-039-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/652a2b068a8d/jgc-10-01-039-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/bd6fe3f5d947/jgc-10-01-039-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/66d62f4ba7ec/jgc-10-01-039-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/0b5c95bd5af4/jgc-10-01-039-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/33963ea98f89/jgc-10-01-039-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/3562414fd7ee/jgc-10-01-039-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/1b8c4ed109b4/jgc-10-01-039-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/4612e501d4bf/jgc-10-01-039-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/0ab94a198a0d/jgc-10-01-039-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/652a2b068a8d/jgc-10-01-039-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/bd6fe3f5d947/jgc-10-01-039-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/66d62f4ba7ec/jgc-10-01-039-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/0b5c95bd5af4/jgc-10-01-039-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/33963ea98f89/jgc-10-01-039-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/3562414fd7ee/jgc-10-01-039-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/1b8c4ed109b4/jgc-10-01-039-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d91/3627714/4612e501d4bf/jgc-10-01-039-g009.jpg

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