Little Known Techniques To Dominate Thanks To Tanespimycin

In control conditions, APD90 in WT and Scn5a+/? were significantly larger than the corresponding atrial effective refractory period (Fig. 8Aa and Ba). This difference was larger in the WT group compared with the Scn5a+/? group. Wild-type hearts thus showed larger positive critical intervals compared with Scn5a+/? hearts (8.8 versus 6.1 ms, respectively; P= 0.03), as reflected in the shaded area of WT and Scn5a+/? AP waveforms observed before introduction of flecainide selleck kinase inhibitor or quinidine. Flecainide significantly prolonged the APD90 in WT (Fig. 8Ab) but not in Scn5a+/? hearts (Fig. 8Bb), but it significantly increased atrial effective refractory period in both groups, as described earlier (see Fig. 7). The resulting negative critical intervals were ?35.3 and ?22.5 ms in WT and Scn5a+/? hearts, respectively (P Adenosine while the position of the dashed vertical line denoting the APD90 moved only slightly to the right in the case of the WT or remained virtually unchanged in the Scn5a+/?. In common with flecainide, quinidine prolonged APD90 values (P selleck inhibitor (Stokoe et al. 2007a,b). Atrial arrhythmic properties may not be simply predictable from their corresponding ventricular properties (Gray & Jalife, 1998) even with mutations involving the same ion channel type. The atria and ventricles show distinct developmental, structural and physiological characteristics and patterns of ion channel expression leading to different action potential waveforms (Tabibiazar et al. 2003; Gaborit et al. 2007). These could potentially result in different phenotypic manifestations of a Brugada syndrome-like change.