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EFFECTS OF ADRENALINE AND NORADRENALINE ON ATRIAL FIBRILLATION PRODUCED BY ACETYLCHOLINE: WITH OBSERVATIONS ON THE MECHANISM OF FIBRILLATION
Author(s) -
Sharma P. L.
Publication year - 1964
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1964.sp001713
Subject(s) - acetylcholine , atrial fibrillation , fibrillation , medicine , atrial flutter , methacholine , cardiology , stimulation , sinus rhythm , atrium (architecture) , anesthesia , lung , respiratory disease
The effect of adrenaline and noradrenaline on atrial fibrillation produced by acetylcholine was studied in intact anæsthetized dogs. In addition, some observations were made concerning the mechanism of the fibrillatory activity of acetylcholine. Atrial stimulation at high rates during adrenaline and noradrenaline infusion produced flutter which persisted for several minutes after the stimulation ceased in four out of fourteen experiments. Simultaneous infusion of adrenaline or noradrenaline enhanced the fibrillatory activity of acetylcholine in all experiments. Topical application of acetylcholine or methacholine to a part of the atrium, coupled with brief atrial stimulation at high rate produced fibrillation which was confined to the treated area, elsewhere flutter was recorded. When this treated area was functionally isolated from the body of the right atrium with a clamp, the arrhythmia persisted in the isolated part, while elsewhere sinus rhythm returned. Also, brief atrial stimulation applied to the right atrial appendage, after topical application of methacholine, produced fibrillation which was confined to the isolated area. The mechanism of fibrillation has been discussed. It has been concluded that the cause of fibrillation resides in the atrial myocardium treated with acetylcholine, and not in the nodal tissues. Experimental observations support the concept of re‐entrant excitation as the cause of fibrillation.