Previous studies have demonstrated that acetylcholine (ACh) and gentle trauma to the atrium induce episodes of atrial fibrillation (AF) lasting 4 to 5 minutes in pigs and canines. Our current study investigated whether this method could be used in rabbits. The left atria of three 4 kg New Zealand white rabbits (Oryctolagus cuniculus) were exposed via a left thoracotomy. Direct application of a 1:100 ACh solution [Miochol-E] accompanied with gentle stroking of the tissue was used in an attempt to produce AF. Direct observation of the atrial surface and an electrocardiogram were used to monitor heart rhythm. We were unable to induce episodes of AF in any of the animals despite numerous attempts with varying amounts of ACh. Bradycardia was eventually observed in each animal, in conjunction with premature ventricular contractions. After approximately 25 minutes of exposure to the ACh, all three animals displayed visual evidence of ischemia of the left atrium and ventricle. The probable explanation for the inability to induce AF in this small-sized animal species is a lack of critical mass of atrial tissue to support such an arrhythmia. However, different arrays of cholinergic receptors do exist between various species, which might provide an alternate explanation. The balance of ACh receptors in the rabbit simply may not be as propitious for this purpose. The ischemia noted during our experiments may be related to the relatively large dose of ACh in relation to the relatively small coronary artery mass in the rabbit. In a number of species, including humans, ACh is a recognized inducer of coronary artery spasm.
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