Paradoxical Cardiac Rhythm in Rat Pups as a Possible Analog of the Sick Sinus Syndrome

Abstract

Experiments with simultaneous recordings of ECG, electrogram of myocardial fibers of the right ventricle and neurogram of the right branch of vagus or sympathetic nerves were carried out on 3–18-day old rat pups. The electric activity recordings were performed under both in vivo and in situ conditions at unilateral or bilateral pneumothorax. It is established that the change in the cholinergic system activation level produced prior to pneumothorax decelerates the rhythm of cardiac contractions (CC) and induces periods of more frequent CC. After pneumothorax, this syndrome becomes more pronounced. The periods of alternation of the slow and fast rhythms may last for up to 1–2 min. The development of the pathological process leads to development of the sino-auricular and atrio-ventricular blocks. There appears a pattern of CC changes and complexes of the ventricular electric potentials that occur in decasecond and then in minute rhythms and are separated by periods of total asystole or preserved potentials of atrial excitation. When the electrograms of myocardium were recorded in rat pups under conditions of bilateral pneumothorax without any pharmacological intervention, it was possible to see a distortion of the sinus rhythm of CC developing for 2–2.5 h after respiration arrest and similar to the above-described distortion. The appearance and development of the phenomenon of the atypical cardiac rhythm is not directly related to the firing patterns of vagus and sympathetic nerves. At the same time, a correlation is clearly seen between the amplitude–frequency modulation of CC and discharges of vagus. A contraction of groups of respiratory muscles lasts for up to 30 min after pneumothorax, with occasional discharges seen in neurogram even after the complete immobilization of the animal. The development of the pathological process reveals a certain similarity with the phenomenon described in literature as the sinus node syndrome (tachy–bradycardia syndrome, TBS). Based on analysis of the cardiac rhythm transformation, it is suggested that the clinical TBS is a consequence of recapitulation, i.e., a successive release of ancient rhythms of excitation due to an impair of regulatory mechanisms.