Transient ventricular fibrillation and myosin heavy chain isoform profile.

The present paper deals with spontaneous ventricular defibrillation in mammals and the possibility to facilitate its occurrence. Clinical and experimental evidence suggest that in the majority of cases, ventricular fibrillation (VF) is permanent, requiring defibrillation by electric shock. However, a growing number of reports show that VF can terminate spontaneously in various mammals, including human beings.

Adaptation of the heart to hypertension is associated with maladaptive gap junction connexin-43 remodeling.

We hypothesized that hypertension-related myocardial remodeling characterized by hypertrophy and fibrosis might be accompanied by cell-to-cell gap junction alterations that may account for increased arrhythmogenesis. Intercellular junctions and expression of gap junction protein connexin-43 were analyzed in rat heart tissues from both spontaneous (SHR) and L-NAME model of hypertension. Isolated heart preparation was used to examine susceptibility of the heart to lethal ventricular fibrillation induced by low potassium perfusion.

Acute, nongenomic effect of thyroid hormones in preventing calcium overload in newborn rat cardiocytes.

In this study, we examined the acute effects of thyroid hormones (TH) T(3) and T(4), leading to improvement of myocardial function through activation of Ca(2+) extrusion mechanisms and, consequently, prevention of intracellular calcium overload. Extracellular calcium elevation from 1.8 to 3.

Enhanced connexin-43 and alpha-sarcomeric actin expression in cultured heart myocytes exposed to triiodo-L-thyronine.

This study examined whether triiodo-L-thyronine (T3) affects the expression of the major intercellular channel protein, connexin-43, and contractile protein alpha-sarcomeric actin. Cultured cardiomyocytes from newborn rats were treated on day three in culture with 10 or 100 nM T3 and examined 48 and 72 h thereafter. Treated and untreated cells were examined by immunofluorescence and electron microscopy.

Modulation of intracellular Ca(2+) concentration by tedisamil, a class III antiarrhythmic agent, in isolated heart preparation.

New class III antiarrhythmic/defibrillating compound tedisamil was shown to facilitate termination of atrial and ventricular fibrillation in experimental as well as clinical conditions. However, class III-related inhibition of K(+) current associated with prolongation of repolarization can not solely explain its defibrillating ability. Following recent findings it was hypothesized that defibrillating effect of tedisamil is likely due to its sympathomimetic feature linked with modulation of intracellular calcium.