The initial reduction of Ito-related molecules, such as the expression levels of Kv4.2, 1.5, frequenin and KChIP2, and the prolongation of MAPD are considered to be a key mechanism of ventricular remodeling and cause the characteristic clinical findings in EAM in the acute inflammatory phase and chronic DCM phase.

Evaluation of Electrophysiological PropertiesTo achieve a stable condition, each dog was allowed to recover for 7 days after the initial surgical procedure without any pacing. Then, rapid atrial pacing (400 beats/min) was initiated and continued for 2 weeks (rapid pacing phase). This pacing was performed at an output of 4-fold the diastolic threshold and a pulse width of 2 ms. After this continuous rapid pacing, the pacing was ceased, and each dog was allowed to recover for 1 week (recovery phase). On days 0, 3, 7, 10 and 14 during the rapid pacing phase, the rapid pacing was stopped temporarily to evaluate the atrial Background The effect of bepridil, a multichannel blocker, on atrial electrical remodeling was evaluated in a canine rapid atrial stimulation model. Methods and ResultsIn 10 beagle dogs, the right atrial appendage (RAA) was paced at 400 beats/min for 2 weeks. The atrial electrophysiological parameters, including effective refractory period (AERP), were evaluated at three atrial sites: RAA, the right atrium close to the inferior vena cava (IVC) and the left atrium (LA), during the time course of rapid pacing. Five of the dogs were given bepridil (10 mg·kg -1 ·day -1 po). In the control group, AERP was significantly shortened at all atrial sites and the AERP shortening (∆AERP) was larger for the RAA and LA than at the IVC site (p<0.05). In the bepridil group, ∆AERP was smaller than that of the controls at all atrial sites, and the AERP started to return slowly to the pre-pacing level in the second week, regardless of the continuation of rapid pacing. Conclusions In a canine rapid atrial stimulation model, bepridil suppressed AERP shortening. Bepridil might have a reverse electrical remodeling effect, at least for AERP shortening, because it showed slow recovery of AERP in the subacute phase of rapid atrial pacing. (Circ J 2006; 70: 206 -213)

By using a dentifrice or toothpaste for sensitive teeth, the brushing-induced effects on dentinal tubule occlusion and abrasion of human sound dentin were investigated with a scanning electron microscope and a scanning laser microscope. The dentifrice contained diatomaceous earth and silica as abrasives and strontium chloride hexahydrate as an active ingredient. Thirty dentin pieces of human premolar teeth with an average of 20% occluded dentinal tubules were attached to resin plates and exposed to the oral cavities of five adult subjects for 2, 4, and 8 weeks. Brushing with and without dentifrice was performed 1 min per day, respectively. Brushing with the dentifrice gradually decreased the mean average of occluded tubules from about 91 to 77% during 2 to 8 weeks, although there were no significant differences among the individual values. However, the mean abrasive loss of the dentin surfaces brushed with dentifrice significantly increased from about 52 to 143 microm in depth. The brushed surfaces of the dentin showed a rough topography with numerous toothbrush scratches but no organic pellicle was found. On the other hand, brushing without dentifrice caused about 99% of the dentinal tubules to occlude in 2 and 4 weeks and 100% in 8 weeks. The brushed dentin surfaces at 8 weeks were entirely covered with organic pellicle containing fine mineral granules derived from saliva, and the abrasive loss was about 1.4 microm in mean depth. Such results indicate that brushing with abrasive dentifrices for sensitive teeth remarkably erodes dentin, and suggest that the brushing should cause the dentinal tubules to open again for a certain period of time.

Shortening of the FCL during a relatively long-term follow-up period was observed in patients with PAF.

SummaryIt has been reported that K-ATP channel openers have a cardioprotective effect in acute ischemia as a pharmacological preconditioning effect. In the present study, the chronic effects of clinical K-ATP channel openers, ie, nicorandil (Nic) and mexiletine (Mex), on cardiac function were evaluated in a rat model of experimental autoimmune myocarditis (EAM). Nicorandil (3 or 10 mg/kg/day) or Mex (10 or 25 mg/kg/day) was administered to the EAM rats, and the effects were compared with those in untreated EAM rats (control EAM) and sham rats without EAM on day 21 (acute phase) or day 60 (chronic phase). In the acute phase, the control EAM rats exhibited a reduced left ventricular ejection fraction (LVEF) and prolonged monophasic action potential duration (MAPD). Neither drug had an affect on the LVEF or degree of myocarditis, but Mex 25 mg suppressed the MAPD prolongation. In the chronic phase, EAM+Nic and EAM+Mex 25 mg exhibited a higher LVEF than the control EAM. Although the control EAM exhibited sustained MAPD prolongation, the other groups showed recovery of the MAPD in the chronic phase. The mitochondorial redox state was lower in the control EAM than in the sham, and EAM+Nic exhibited a similar level of the redox state as the sham in the chronic phase. Nicorandil exhibited a cardioprotective effect through the protection of mitochondrial function. Mexiletine exhibited a cardioprotective effect possibly through a reduction in the calcium overload by shortening the MAPD in the acute phase. (Int Heart J 2012; 53: 139-145)