The heart cell: some metabolic aspects of cardiac arrhythmias.
The maintenance of normal electrical activity in the myocardium is an ATP-dependent process. Consequently failure to maintain the tissue reserves of ATP above a critical level, as occurs during ischaemia and post ischaemic reperfusion, results in the development of ionic imbalance. The ions involved include Na+, K+, Mg2+. Under conditions of low flow ischaemia an accumulation of K+ in the T-tubules may account for the genesis of some of the arrhythmias that occur during the ischaemic episode. Electrical uncoupling, another later event in an ischaemic episode, is probably due to an intracellular accumulation of Ca+. The contribution of an altered pattern of electrolyte distribution to the genesis of arrhythmias during myocardial ischaemia is discussed, with reference to the mechanisms whereby these ionic imbalances can be minimized or prevented.
D000200:Action Potentials; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006801:Humans; D007473:Ion Channels; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D007473:Ion Channels; D000255:Adenosine Triphosphate; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D002118:Calcium