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 Rabbitswith occlusion of th...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 Rabbitswith occlusion of the left anterior descending coronary arterywere 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 cellswere recorded using whole-cell patch clamps. Results Comparedwith 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 (Ito), the rapidly activated omponent of delayed rectifier potassium current (IKr), the slowly activated component of delayed rectifier potassium current (IKs), and the L-type calcium current (ICaL) were significantly altered in NGF + HMI cardiomyocytes compared with HMI and control cells. Conclusions Our results suggest thatNGF treatment significantly prolongsAPDinHMI cardiomyocytes and that a decrease in outward potassium currents and an increase of inward Ca2+ current are likely the underlying mechanism of action.展开更多
基金We are grateful to the support of Dr. Lei Yuan and Shao-Shao Zhao for their technical assistance. This work was supported in part by China Postdoctoral Science Foundation Province, China
文摘ObjectivePrevious 研究证明组织缺氧 preconditioning 能保护心脏的功能免于随后的心肌的梗塞损害。然而，在在心肌的梗塞以后室的左的组织缺氧的效果仍然是不清楚的。这研究因此试图调查在在兔子柱子的左室的改变上训练的组织缺氧的效果心肌的 infarction.MethodsAdult 男性兔子随机被划分成三个组：那么组织(假冒操作) ，组 MI (心肌的梗塞仅仅) 并且组 MI-HT (加组织缺氧训练的心肌的梗塞) 。心肌的梗塞被左室的分支结扎导致。训练的组织缺氧在一个比重低於脑脊髓液的房间被执行(在 4000 m 的高度有相等的状况， F <sub > i </sub > 为 1 h/day 的 O <sub>2</sub>14.9%) ，为四个星期的 5 天 / 星期。在端点，在血浆的脉管的 endothelial 生长因素(VEGF ) 被测量。梗塞尺寸和毛状的密度被组织学检测。左室的改变和功能被 echocardiography.ResultsAfter 估计 4 星期的实验，与这个组相比那么，在组 MI 的血浆 VEGF 层次(130.27 ±；18.58 pg/mL， P <；0.01 ) 并且 MI-HT (181.93 ±；20.29 pg/mL， P <；0.01 ) 显著地被增加。在组 MI-HT 的梗塞尺寸(29.67%±；7.73%) 显著地被死亡，当时它的毛状的密度(816.0 ±；122.2/mm <sup>2</sup>) 显著地被增加。为组 MI 和 MI-HT，而左室的喷射部分被减少，左室的结束心脏舒张、结束收缩的尺寸被增加。与组 MI 相比，然而，组 MI-HT 减少了留给室结束心脏舒张(15.86 ±；1.09 公里， P <；0.05 ) 并且结束收缩的尺寸(12.10 ±；1.20 公里， P <；0.01 ) 显著地并且改进左室的喷射部分(54.39 ±；12.74 公里， P <；0.05 ) 训练可以改进的 .ConclusionHypoxia 让室的功能和还原剂与 MI 在兔子经由 angiogenesis 改变。
文摘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 Rabbitswith occlusion of the left anterior descending coronary arterywere 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 cellswere recorded using whole-cell patch clamps. Results Comparedwith 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 (Ito), the rapidly activated omponent of delayed rectifier potassium current (IKr), the slowly activated component of delayed rectifier potassium current (IKs), and the L-type calcium current (ICaL) were significantly altered in NGF + HMI cardiomyocytes compared with HMI and control cells. Conclusions Our results suggest thatNGF treatment significantly prolongsAPDinHMI cardiomyocytes and that a decrease in outward potassium currents and an increase of inward Ca2+ current are likely the underlying mechanism of action.
