Administration of neurotensin against the background of sinus arrhythmia caused by burst stimulation of the vagus nerve in cats restores synchronization of the cardiac and vagal rhythms or modulates the proportion between them. This either stops the arrhythmia or changes its parameters. The effects of the peptide are similar to those of epinephrine and are abolished by 13-adrenoreceptor blockage.
Key Words: vagus nerve; sinus arrhythmia; neurotensin; epinephrineThe effect of the vagus nerve (VN) on the heart is modulated by peptides localized in neurons of the intracardial nervous system [2,9], For instance, neurotensin (NT) considerably changes the dynamics of controlled bradycardia caused by synchronization of the cardiac rhythm with the frequency of bursts delivered to the VN [3]. The aim of the present study was to investigate the effect of this peptide under conditions of desynchronization of the vagal and cardiac rhythms, in particular in sinus arrhythmia [4].
MATERIALS AND METHODSExperiments were carried out on 22 cats weighing 2.5-3.5 kg narcotized intraperitoneally with a Chloralose-Nembutal mixture (75 and 15 mg/kg, respectively), and artificially ventilated. The right VN was divided in the neck and its peripheral end was stimulated by bursts of 6 square pulses. The duration and frequency of the pulses in a burst were 2 msec and 40 Hz; the amplitude was 5-6 threshold values. The amplified ECG was recorded by means of a unipolar probe inserted through the femoral vein into the right atrium; the P wave of the ECG triggers the
RESULTSThe duration of the cardiac cycle after dissection of the fight VN was 329.4+9.8 msec. Stimulation of VN resulted in bradycardia; within a certain range of burst repetition rate (from 1.44+0.09 to 1.78+0.1 Hz) the heartbeats became synchronous with the vagal stimuli (Fig. 1) allowing for strictly controlled modulation of the cardiac cycle duration (from 557.1+15.4 to 694.3+18.2 msec). These limits were specified as the upper and lower boundaries of the synchronization interval. A repetition rate exceeding this interval led to desynchronization and development of sinus arrhythmia. Sinus arrhythmia arose from disturbed parallelism between the repetition rate of bursts delivered to VN and the lengthened heart rate, so that position of the vagal stimulus varied from cycle to cycle. For instance, in above-synchronization arrhythmia, the burst repetition rate exceeded the heart rate and the next vagal stimulus
