The excitation of the vagus nerve can significantly shorten AERP, while also increasing the dispersion of AERP, providing opportunities for multi wavelet reentry, leading to the susceptibility and stability of AF. Schuessler et al. induced atrial fibrillation (AF) by stimulating the vagus nerve: a routine disinfection cloth was placed, and a 6-8cm incision was made between the 4-5 ribs on the right side of the sternum. After thoracotomy, the heart was fully exposed, and the pericardium was cut open and hung on the chest wall. Multiple electrode mapping catheters were placed in the right atrial appendage, right ventricle, coronary sinus, and His bundle, respectively. Basket shaped electrodes were inserted at the junction of the left and right pulmonary arteries and the main pulmonary artery, and at the junction of the left atrium and pulmonary vein. The position and output voltage of the electrodes were adjusted to stimulate the vagus nerve. The effective stimulation site and intensity of the vagus nerve plexus were reduced by 50% in sinus rhythm. Then, the catheter was fixed, and the vagus nerve plexus was stimulated at a frequency of 20Hz and a pulse width of 0.1 milliseconds with a voltage of 1-40V for 50 milliseconds.
Histological examination shows that the cardiac fat pad contains abundant autonomic nerve plexuses, and the bilateral vagus nerves converge on these autonomic nerve plexuses before innervating the atrium, and then emit axons to innervate the atrium. Therefore, electrical stimulation of the fat pad and pulmonary veins can also establish an AF model. Hayashi et al. separated, fixed, and severed the vagus nerve in the neck of dogs, and placed Teflon coated metal electrodes at the cardiac end of the nerve to stimulate efferent nerves. At the same time, the subclavian ganglion was also separated and excised. During continuous bilateral vagus stimulation, atrial trigger stimulation with a cycle of 90-120 milliseconds can induce AF. The important mechanism by which vagus nerve stimulation induces atrial fibrillation is that vagus nerve excitation can significantly shorten the wavelength of AERP and excitation conduction, allowing the atrium to accommodate more reentry waves simultaneously; And increase the dispersion of effective refractory period in the atrium, making AF easier to induce and maintain. This type of AF model can be used as a fixed model for studying autonomic nervous system tension imbalance AF and focal paroxysmal AF.