ABSTRACT
Excitation of vagal nerves results in the emergence of temporarily inexcitable regions in atria. The fact is shown using microelectrode techniques and the mapping of excitation on frog atria isolated together with vago-sympathetic trunks. These regions serve as unidirectional block and functional obstacle provoking reentry-type arrhythmia. The mechanism is defined in terms of a two-dimensional mathematical model which elements were axiomatically set to have the following states: rest, excitation, refractoriness, and vagal inexcitability. With the help of the model we have explained the mechanism of initiation, development and termination of neurogenic tachyarrhythmia. Using micro electrode techniques on an isolated rabbit right atrium we have shown that during intramural nerve excitation as well as in the presence of Ach, there occur inexcitable loci within sinoatrial node (SAN). Probability of development of inexcitability negatively correlates with the velocity of AP upstroke of SAN cells. At maximum upstroke rates higher than 3 V/s, 80 to 90% trials of cholinergic interference resulted in inexcitability. At upstroke rates higher than 12 V/s, inexcitability was not observed. Unlike in amphibians, cholinergically induced inexcitability was not observed in rabbit and canine atria. Cholinergically induced inexcitability in central SAN cells has been simulated with the help of a computer model. The model provides a detailed description of transmembrane current and intracellular ion flows. The computed data are in good agreement with available experimental results.
