The role of biochemical factors in ventricular dysrhythmia accompanying ischemia.
Early malignant ventricular dysrhythmia induced by ischemia appear to depend on electrophysiological changes predisposing toward reentry. These changes are not readily explicable in terms of direct responses to hypoxia alone. Data from several laboratories make it increasingly clear that regional, heterogenous accumulations of noxious ions and metabolites play an important role. In addition to previously recognized factors including potassium, lactate, and hydrogen ion, both free and esterified fatty acid derivatives and metabolites of membrane phospholipids, particularly lysophosphoglycerides, have been implicated as potential mediators. Elucidation of the biochemical mechanisms responsible is of particular importance to development of prophylactic and therapeutic interventions with the needed specificity to be effective in reducing the incidence and severity of malignant ventricular dysrhythmia induced by ischemia and hence of sudden death.
D000200:Action Potentials / Q000187:drug effects; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D001706:Biopsy; D003327:Coronary Disease / Q000097:blood / Q000150:complications*; D000242:Cyclic AMP / Q000032:analysis; D005110:Extracellular Space / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000032:analysis; D005994:Glycerophosphates / Q000032:analysis; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D066298:In Vitro Techniques; D007773:Lactates / Q000097:blood
D000889:Anti-Arrhythmia Agents; D005230:Fatty Acids, Nonesterified; D005994:Glycerophosphates; D007773:Lactates; D000242:Cyclic AMP