Electrical instability of the heart in acute local myocardial ischaemia: pathogenesis and experimental prevention.
The pathogenesis of electrical instability of tissue in the earliest phase of ischaemia is well known. Convincing results in the prevention of ventricular fibrillation at this stage have been obtained only by agents inhibiting sympathetic activation of the heart, or by agents significantly prolonging the refractory period of heart cells. On the other hand, it was documented that sodium channel inhibitors are not suitable for prevention of electrical instability in the early phase of ischaemia and can, on the contrary, aggravate it. A question which is still unresolved and deserves further research is the effect of calcium channel inhibitors and of agents acting directly on the metabolism of ischaemic tissue.
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D003327:Coronary Disease / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D004285:Dogs; D004594:Electrophysiology; D014290:Metipranolol / Q000627:therapeutic use; D016293:Moricizine; D009206:Myocardium / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000502:physiology; D010640:Phenothiazines / Q000627:therapeutic use; D014288:Trimecaine / Q000627:therapeutic use; D014693:Ventricular Fibrillation / Q000503:physiopathology*
D000889:Anti-Arrhythmia Agents; D018377:Neurotransmitter Agents; D010640:Phenothiazines; D016293:Moricizine; D014288:Trimecaine; D014290:Metipranolol