Remodeling of gap junctional channel function in epicardial border zone of healing canine Infarcts

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 (G(j)) accompany the increased anisotropy. Ventricular cell pairs were isolated from EBZ and normal hearts (NZ). Dual patch clamp was used to quantify G(j). At a transjunctional voltage (V-j)of +10 mV, side-to-side G(j) of EBZ pairs (9.2+/-3.4 nS, n=16) was reduced compared with NZ side-to-side G(j) (109.4+/-23.6 nS, n=14, P<0.001). G(j) of end-to-end coupled cells was not reduced in EBZ. Steady-state G(j) 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 V-j 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.