No abstract available.
Doxorubicin* ; Myocytes, Cardiac*

No abstract available.
Extracellular Space* ; Ischemia* ; Myocytes, Cardiac*

Autophagy ; Humans ; Myocytes, Cardiac ; Ventricular Remodeling

Apoptosis ; Inhibitor of Apoptosis Proteins ; Myocytes, Cardiac ; cytology

Adult Stem Cells ; Myocytes, Cardiac ; cytology

Studies have demonstrated that the occurrence of a variety of arrhythmias presents an obvious circadian rhythm,which may be regulated by circadian rhythm genes.Circadian cycle and light stimulation can affect circadian rhythm genes and proteins,which constitute a transcription-translation loop that can regulate the ion channels in myocardial cell membrane through nervous-humoral regulation and changes in central clock-sub-clock gene expression,thereby modulating arrhythmia.This article reviews the molecular basis,mechanism,and performance of circadian rhythm in regulating arrhythmia.
Humans ; Circadian Rhythm/genetics* ; Myocytes, Cardiac ; Arrhythmias, Cardiac

Ischemia is the most common and important cause of injury to cardiomyocytes. Acute ischemia causes profound derangement of the cellular energetics and metabolism, and this ultimately leads to cell death. Experimental studies have demonstrated the presence of an endogenous protective mechanism that can diminish or delay cell death from ischemic insult; this is known as ischemic preconditioning. In this review, we summarize the recent knowledge of the cellular biology of acute ischemic injury and also signaling mechanisms of cardioprotection that are involved in preconditioning. Further, we briefly discuss the clinical implications.
Cell Death ; Ischemia* ; Ischemic Preconditioning ; Metabolism ; Myocytes, Cardiac*

Molecular Probe Techniques ; Myocytes, Cardiac ; physiology ; Regeneration ; Stem Cells

OBJECTIVETo explore the possible relationship between the ultrastructural characteristics of pulmonary veins and the pathogenesis of atrial fibrillation originating from pulmonary veins.

METHODSThe pulmonary veins from domestic pigs were serially sectioned (2 mm) transversely along the vessels. The odd number sections were fixed in 10% phosphate buffered formalin solution and the even number sections were fixed in 3% Glutaral for further electron microscopy observations.

RESULTSTwo cell types were found in the pulmonary veins of pigs. One cell type was the P-like cells that had an empty-appearing cytoplasm containing only sparse myofibrils and small mitochondria, both of which were randomly distributed. Another cell type was slender transitional cells with plenty of longitudinally displayed myofibrils.

CONCLUSIONP-like cells in the pig pulmonary veins were found using electron microscopy in this study and ectopic beats from P-like cells in the myocardial sleeves in the pulmonary veins might be responsible for atrial fibrillation originating from pulmonary veins.

OBJECTIVECurrents contributing repolarization in rabbit ventricular myocyte are very complex since the I(To.s) covers almost the whole repolarization phase of the action potential. The other components of repolarizing currents, as I(Kr) and I(Ks) are small. The purpose of this study is to investigate whether or not there are other currents in rabbit ventricular repolarization.

METHODSIon currents of rabbit ventricular myocyte were recorded using the whole-cell patch-clamp technique.

RESULTSIn the present work, an nonselective cation current was identified by replacing the K(+) with Cs(+) in the bathing and pipette solutions. The outward current elicited by depolarizing potentials could be inhibited by Gd(3+), an effective inhibitor of nonselective cation currents. Depleting Ca(2+) and Mg(2+) in the bathing solution, the amplitudes of this outward current increased by 40%-116% at +60 mV, and adding 2 micromol/L insulin to the solution (with normal concentration of Ca(2+) and Mg(2+) in Tyrode's solution), the amplitude increased by 30%-60% at +60 mV.

CONCLUSIONIt is suggested that a nonselective cation current in rabbit ventricular myocytes may play an important role in the repolarization of the action potential in rabbit ventricle. Changes of nonselective cation current will lead to induce or inhibit arrhythmia.