Yao Jian-An, Hussain Wajid, Patel Pravina, Peters Nicholas S, Boyden Penelope A, Wit Andrew L
Dept of Pharmacology and Center for Molecular Therapeutics, Columbia University, 630 West 168th St, PH7W, New York, NY 10032, USA.
Circ Res. 2003 Mar 7;92(4):437-43. doi: 10.1161/01.RES.0000059301.81035.06. Epub 2003 Jan 30.
The epicardial border zone (EBZ) of canine infarcts has increased anisotropy because of transverse conduction slowing. It remains unknown whether changes in gap junctional conductance (Gj) accompany the increased anisotropy. Ventricular cell pairs were isolated from EBZ and normal hearts (NZ). Dual patch clamp was used to quantify Gj. At a transjunctional voltage (Vj) of +10 mV, side-to-side Gj of EBZ pairs (9.2+/-3.4 nS, n=16) was reduced compared with NZ side-to-side Gj (109.4+/-23.6 nS, n=14, P<0.001). Gj of end-to-end coupled cells was not reduced in EBZ. Steady-state Gj of both NZ and EBZ showed voltage dependence, described by a two-way Boltzmann function. Half-maximal activation voltage in EBZ was shifted to higher Vj in positive and negative directions. Immunoconfocal planimetry and quantification showed no change in connexin43 per unit cell volume or surface area in EBZ. Decreased side-to-side coupling occurs in EBZ myocytes, independent of reduced connexin43 expression, and is hypothesized to contribute to increased anisotropy and reentrant arrhythmias.
由于横向传导减慢，犬梗死灶的心外膜边界区（EBZ）各向异性增加。间隙连接电导（Gj）的变化是否伴随各向异性增加尚不清楚。从EBZ和正常心脏（NZ）分离出心室细胞对。采用双膜片钳技术定量Gj。在跨连接电压（Vj）为+10 mV时，EBZ细胞对的侧向Gj（9.2±3.4 nS，n = 16）低于NZ细胞对的侧向Gj（109.4±23.6 nS，n = 14，P<0.001）。EBZ中首尾相连耦合细胞的Gj未降低。NZ和EBZ的稳态Gj均表现出电压依赖性，可用双向玻尔兹曼函数描述。EBZ中的半最大激活电压在正负方向上均向更高的Vj偏移。免疫共聚焦平面测量和定量分析显示，EBZ中每单位细胞体积或表面积的连接蛋白43没有变化。EBZ心肌细胞中侧向耦合减少，与连接蛋白43表达降低无关，推测这有助于各向异性增加和折返性心律失常。
