Myocardial cell membrane stabilization and antiarrhythmic action.
Shifts in the normal balance of neurovegetative and hormonal regulations, modifications in the ionic composition of the plasma and pathological changes such as ischaemia, hypoxia and hypercapnia may lead to changes in permeability of the cardiac cell membranes to different ions, resulting in electrophysiological changes. These are: depressed and non-homogeneous conduction of impulses, lack of homogeneity in excitability and recovery of excitability, increased ectopic automaticity, etc. Interaction of these changes may be responsible for the appearance of arrhythmias. Membrane stabilization in a broader sense means a tendency to restore pathologically altered membrane permeability, permitting normal ionic transport through membranes of the heart muscle cells and protecting the heart from arrhythmia. In this sense not only classical membrane stabilizing agents such as quinidine- or lidocaine-type drugs are antiarrhythmic; so are the very heterogeneous group of agents defined as calcium antagonists or the interventions changing the phospholipid composition of the cardiac cell membrane, such as a linoleic-acid rich diet or adjuvant arthritis. Examples of these actions are given in the heart in situ of the anaesthetized dog and in the conscious rat infarction model.
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D002462:Cell Membrane / Q000187:drug effects*; D002463:Cell Membrane Permeability / Q000187:drug effects; D004032:Diet; D004285:Dogs; D008041:Linoleic Acids / Q000494:pharmacology; D009203:Myocardial Infarction / Q000503:physiopathology; D009206:Myocardium / Q000166:cytology*
D000889:Anti-Arrhythmia Agents; D008041:Linoleic Acids