中文摘要：

目的：通过干预神经营养因子p75受体（p75NTR）探讨心肌梗死（MI）后神经过度增生对心肌细胞Ito.f异质性的影响.方法：选日本大耳兔40只随机分为陈旧性心梗（HMI）组、p75NTR激活组、p75NTR抑制组和假手术组，每组10只（n=10）：采用酶解法制备3层心室肌单细胞，利用全细胞膜片钳技术记录电流。结果：在以＋50mV的去极化刺激时，HMI组的Ito.f峰电流密度有所下降，在以p75NTR受体激活后，3层心肌Ito.f峰电流密度的下降更为明显，与假手术组比差异显著（P〈0．05或P〈0．01），其中以中层心肌Ito.f峰电流密度的下降程度最大；而应用p75NTR抑制剂后，下降的程度降低，与假手术组比无明显差异：与对照组相比，中层心肌细胞的Ito.f电压依赖性失活曲线在p75NTR激活组及HMI组均向负移，p75NTR抑制组得以恢复：Ito.f通道关闭态的T值在4组的3层心肌细胞间存在明显差异，即p75NTR激活组及HMI组失活较快，尤以p75NTR激活组为甚，p75NTR抑制组的关闭态失活与对照组接近。结论：p75NTR激活后，3层心肌Ito.f峰电流密度下降明显，尤其以中层细胞为甚，此可能是导致跨室壁复极离散度显著增加，最终引起心律失常发生的原因之一。

英文摘要：

AIM： To elucidate the effect of neurotrophin p75 receptor （p75NTR） on the transmural repolarization dispersion of the transient outward potassium current （Ito.f） of three layers of left ventricular myocytes in rabbits with myocardial infarction （MI）. METHODS： Forty Japanese rabbits were divided into four groups： 1 ） HMI group, 2） p75 NTR activation group, 3） p75 NTR inhibition group and 4） sham group. Cardiomyocytes were isolated with enzyme digestion and the currents were recorded by whole-cell patch-clamp technique. RESULTS： Compared with those in the sham group, the densities of Ito.f in the HMI group and p75NTR（ ＋ ） group were significantly reduced （P 〈0.01, n = 10） , especially in midmyocytes. This difference was reduced by inhibitor of p75NTR. Current densities of Ito.f in p75NTR （ - ） group was similar to that in sham group. Compared with that in sham group, the steady-state inactivation curve of Ito.f in the midmyocytes shifted to the negative in p75NTR（ ＋ ） and HMI groups, and no obvious changes were observed in p75NTR（ - ） group. Significant differences were observed in the time constant values of closed-state inactivation of Ito.f in three layers of myocytes among the four groups, and closed-state inactivation was faster in p75NTR（ ＋ ） and HMI groups, especially in p75NTR（ ＋ ） group. The time constant values of closed-state inactivation of Ito.f in p75NTR（ - ） group was similar to that in sham group. CONCLUSIONS： Activation of p75NTR（ ＋ ） reduces the current densities of Ito,f of three layers of myocytes, especially those in midmyocytes, which may result in the increase of transmural repolarization dispersion and incidence of arrhythmia.