Central neurochemical factors related to serotonin metabolism and cardiac ventricular vulnerability for repetitive electrical activity.
Sympathetic neural activity modifies cardiac excitability and lowers the threshold of the vulnerable period for ventricular fibrillation. Sympathetic neural traffic to the heart can be diminished by administering serotonin precursors that localize in the central nervous system. In this study anesthetized dogs were injected with either of the serotonin precursors L-tryptophan or 5-hydroxy-L-tryptophan in conjunction with the monoamine oxidase inhibitor pheneizine and the selective peripheral L-amino acid decarboxylase inhibitor carbidopa. Ventricular vulnerability was evaluated by measuring the repetitive extrasystole threshold. A sustained increase of 50 percent in this threshold resulted only with use of biochemical measures that presumably increase serotonin levels in the central nervous system. Thus neuropharmacologic measures affecting central sympathetic activity alter cardiac vulnerability and may protect against ventricular fibrillation.
D006916:5-Hydroxytryptophan / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002230:Carbidopa / Q000494:pharmacology; D005117:Cardiac Complexes, Premature / Q000139:chemically induced; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000294:innervation*; D008297:Male; D010624:Phenelzine / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism*; D013564:Sympathetic Nervous System; D014364:Tryptophan / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000139:chemically induced
D012701:Serotonin; D014364:Tryptophan; D006916:5-Hydroxytryptophan; D002230:Carbidopa; D010624:Phenelzine