The effect of lidocaine on lysophosphatidylcholine-induced cardiac arrhythmias and cellular disturbances.
The production of arrhythmias in the isolated heart by perfusion with lysophosphatidylcholine has been well documented. However, the role of the lysophospholipid as a physiological factor in the generation of cardiac arrhythmias is not clear. In this study, a pharmacological approach was used to delineate the physiological significance of lysophosphatidylcholine during this cardiac dysfunction. Lidocaine (5-20 mg/L) was found to be effective in the protection of the isolated rat heart from the lysophospholipid-induced arrhythmias at pharmacological concentrations. The effect of lidocaine in the protection of lysophospholipid-induced membrane dysfunction was studied with red blood cells. Lidocaine (2 mg/mL) protected red blood cells from hemolysis in the presence of lysophosphatidylcholine. Lidocaine did not inhibit the binding of the lysophospholipid to the red cell membrane, but inhibited hemolysis in a manner similar to cholesterol. The results are consistent with the postulate that lysophosphatidylcholine is a physiological factor in the pathogenesis of cardiac arrhythmias during myocardial ischemia.
D000418:Albumins / Q000494:pharmacology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control; D002462:Cell Membrane / Q000187:drug effects; D002784:Cholesterol / Q000494:pharmacology; D004562:Electrocardiography; D004910:Erythrocyte Membrane / Q000378:metabolism; D006461:Hemolysis / Q000187:drug effects; D066298:In Vitro Techniques; D008012:Lidocaine / Q000494:pharmacology*; D008244:Lysophosphatidylcholines / Q000037:antagonists & inhibitors / Q000633:toxicity*; D008297:Male; D051381:Rats; D014693:Ventricular Fibrillation / Q000097:blood
D000418:Albumins; D008244:Lysophosphatidylcholines; D002784:Cholesterol; D008012:Lidocaine