Objective: Heart failure in patients and in animal models is associated with action potential prolongation of the ventricular myocytes. Changes in several membrane currents have been already demonstrated to underlie this prolongation. However, information on the two components (I and I ) of the delayed rectifier potassium current (I ) in rapid pacing induced heart failure is lacking. Methods and underly action potential prolongation at physiological cycle length and thereby contribute to arrhythmogenesis in heart failure.

Background-The ionic basis of acquired QT prolongation and torsade de pointes (TdP) unrelated to drugs is not fully understood. Methods and Results-We created a rabbit model with chronic complete atrioventricular block (AVB) (nϭ34), which showed prominent QT prolongation (by 120%), high incidence of spontaneous TdP (71%), and cardiac hypertrophy. Patch-clamp experiments were performed in left ventricular myocytes from 9 rabbits (8 with TdP, 1 without TdP) at Ϸ21 days of AVB and from 8 sham-operated controls with sinus rhythm. Action potential duration was prolonged in AVB myocytes compared with control (ϩ61% at 0.5 Hz, ϩ21% at 3 Hz). Both rapidly and slowly activating components of the delayed rectifier K ϩ current (I Kr and I Ks ) in AVB myocytes were significantly smaller than in control by 50% and 55%, respectively. There was no significant difference in Ca 2ϩ -independent transient outward current (I to1 ). L-type Ca 2ϩ current (I Ca,L ) in control and AVB myocytes was similar in peak amplitude, but the half voltage for activation was shifted to the negative direction (5.9 mV) in AVB myocytes. Voltage dependence of I Ca,L inactivation was not different in control and AVB myocytes. The inward rectifier K ϩ current (I K1 ) significantly increased in AVB myocytes compared with control. Conclusions-In the rabbit, chronic AVB leads to prominent QT prolongation and high incidence of spontaneous TdP. Downregulation of both I Kr and I Ks in association with altered I Ca,L activation kinetics may underlie the arrhythmogenic ventricular remodeling.

This report presents some experimental data that were recorded from 130 impact tests on mild steel pipes in two drop hammer rigs. The pipes were fully clamped across a span which was ten times the corresponding outside pipe diameters which lie between 22 and 324 mm. All of the pipes except five had wall thicknesses of 2 mm approximately and were impacted laterally by a rigid wedge indenter at the mid span, one-quarter span or near to a support. The impact velocities ranged up to 14 m/s and caused various failure modes. Some comparisons between two sets of experimental results indicate that the laws of geometrically similar scaling are almost satisfied over a scale range of approximately five.