Arrhythmias, Cardiac ; pathology ; physiopathology ; Humans ; Purkinje Fibers

Arrhythmias, Cardiac ; physiopathology ; Child ; Electrocardiography ; Humans ; Male ; Tachycardia, Ventricular ; physiopathology

Arrhythmias, Cardiac ; diagnosis ; Electrocardiography ; Heart Ventricles ; physiopathology ; Prognosis

Arrhythmias, Cardiac ; physiopathology ; Electromyography ; methods ; Female ; Humans ; Infant, Newborn ; Male

Arrhythmias, Cardiac ; etiology ; physiopathology ; Humans ; Myocardial Infarction ; physiopathology ; Sympathetic Nervous System ; physiopathology

Malignant arrhythmias and ventricular fibrillation are generally accepted as one of the major causes of death in cardiovascular diseases. Based on the H-H equations, the mathematical model of the cardiac cell action potential consists of the ion channels, pumps, exchangers and transporters that are closely connected with intra- and extra-cellular ion concentrations, the channel's conditions, nerve transductors and drugs. It can build the link between cell electrophysiology and clinical pathophysiology. By altering the cellular environments the computer simulating study on this kind of model can help us look into the electrophysiological changes of the cardiac tissue and even the whole heart and investigate the mechanisms of the cardiac arrhythmias as well. The components of the model and its computer simulating study are introduced in the paper.
Action Potentials ; Arrhythmias, Cardiac ; physiopathology ; Computer Simulation ; Heart ; physiopathology ; Humans ; Models, Cardiovascular ; Ventricular Fibrillation ; physiopathology

Ion channelopathies are the mainly etiopathogenisis of inherited arrhythmia. Those arrhythmia syndromes are commonly caused by ion channel gene mutation, which can be classified as sodium,potassium and calcium ion channel mutation.Changes in the genes encoding for cardiac ion channel subunits produce modification in the function of the channels, and cause the dysfunctions of cardiac electrical activity; and the clinical manifestation is malignant arrhythmia.
Animals ; Arrhythmias, Cardiac ; genetics ; physiopathology ; Channelopathies ; genetics ; physiopathology ; Humans ; Ion Channels ; genetics ; physiology ; Mutation

Aged ; Anthracosis ; physiopathology ; Arrhythmias, Cardiac ; physiopathology ; Case-Control Studies ; Electrocardiography ; Humans ; Middle Aged

Aged ; Arrhythmias, Cardiac ; diagnosis ; physiopathology ; Coal Mining ; Electrocardiography ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; complications ; physiopathology

OBJECTIVETo determine effects of activating protein kinase C (PKC) on ventricular action potential duration restitution (APDR) and Burst stimulus induced arrhythmia in Langendorff-perfused rabbit hearts.

METHODSMale rabbits were equally divided into three groups randomly: control group (Tyrode's solution perfusion), PKC agonist phorbol-12-myristate-13-acetate (PMA, 100 nmol/L) group and PKC inhibitor bisindolylmaleimide (BIM, 500 nmol/L) group. Thirty minutes after perfusion, the monophasic action potential (MAP) and effective refractory period (ERP) were determined in right basal ventricle (RB), right apex (RA), left basal ventricle (LB) and left apex (LA) of all the animals, and APDR curve was drawn. Burst stimulus method was used to induce ventricular arrhythmia in perfused rabbit hearts; Real-time PCR was used to detect the mRNA expression of PKC in four different areas of ventricle.

RESULTSCompared with the control group, the ERP, 90% of monophasic action potential duration (MAPD(90)) and ERP/MAPD(90) were significantly shortened (all P < 0.01), the max slopes (S(max)) of APDR curve were significantly steeper (RB: 1.22 ± 0.23 vs. 0.65 ± 0.19; RA: 2.99 ± 0.29 vs. 1.02 ± 0.18; LB: 1.84 ± 0.21 vs. 0.85 ± 0.12; LA: 4.02 ± 0.32 vs.1.12 ± 0.23, all P < 0.01) and the incidences of ventricular arrhythmia were significantly increased in the PMA group. All parameters were similar between the BIM group and the control group (all P > 0.05).

CONCLUSIONActivating PKC could enhance the max slopes of APDR curve at various ventricular areas and subsequently increase arrhythmia susceptibility in Langendorff-perfused rabbit hearts.

Action Potentials ; Animals ; Arrhythmias, Cardiac ; physiopathology ; Heart ; drug effects ; physiopathology ; Male ; Protein Kinase C ; pharmacology ; Rabbits