Depression of atrioventricular sensitivity in the dog by successive brief bursts of vagal stimulation.

Abstract

SUMMARY When identical, successive single vagal stimulations, separated in time (T) by 2-60 seconds, are applied in the dog, the peak change in atrioventricular conduction time for the second stimulus, AAV 2 , is less than that of the first, AAV,, that is, the ratio AAV 2 /AAV, < 1.0 (the mean minimum AAV 2 /AAV, = 0.52). It was further determined that at any one given T, the actual value of AAVj/AAV, also was a function of the first stimulus amplitude. The same dependence of A AV 2 /AAV, on the first stimulus amplitude was found when the amplitude was varied either by (1) changing the number of vagal fibers stimulated for both the first and second response, but at a constant AD (the delay in the cardiac cycle at which the stimulus was given), or (2) by stimulating the same number of fibers but changing AD for both the first and second response. Also the same characteristic of AAV 2 /AAV, plotted vs. T was found either (1) when both the first and second responses were produced by stimulation of the same nerve, or (2) when stimulation of the nerve from one side produced the first response and the alternate side the second response. These data suggest that the reason for this AAVj/AAV, time-dependent effect lies in changes in receptor responsiveness or in acetylcholine inactivation, but not in mechanisms purely internal to the nerve terminal associated with synthesis, storage, or release of acetylcholine.WHEN A TEST stimulus is applied to the vagus nerve after a conditioning stimulus, the increment in cardiac cycle length or atrioventricular conduction time produced by the test stimulus may be considerably less than that produced by the first (conditioning) stimulus. This has been found both for a single stimulus 1 and for pulse trains. 2 -3 In this study these conditioning phenomena were explored in an effort to analyze the mechanism by which they are produced. MethodsExperiments were conducted on 18 mongrel dogs (10-15 kg) of both sexes; 16 yielded satisfactory results (in the other two dogs the responses to a repeated standard test stimulation of the vagus decayed to too great an extent with time to be usable). The dogs were anesthetized with morphine sulfate (2 mg/kg, im), followed 30 minutes later by chloralose dissolved in polyethylene glycol (75 mg/kg, iv).Both cervical vagosympathetic trunks were dissected free from surrounding tissues, crushed, and ligated centrally. Either the left trunk, or both left and right trunks, were connected to a bipolar shielded electrode (Grass) at a point distal to the ligature. /9-Adrenoreceptors were blocked with propranolol (1.0 mg/kg, iv) to abolish the effects of stimulation of cardiac adrenergic fibers contained in the vagosympathetic trunk. Adequacy of blockade was confirmed in selected dogs at 1-hour intervals by noting the absence of cardiac responses to periodic maximal stimulation of the right stellate ganglion. The heart was paced continually throughout the experiment at a rate just above the spontaneous rate; usually the paced cycle length ranged from 400 to 550...

The fade of the response to acetylcholine at the rabbit isolated sino‐atrial node.

“…Fade manifested as an increase in the heart rate has been seen during prolonged trains of vagal stimuli in the heart in situ (Burke & Calaresu, 1972;Martin et al 1982), and although this may have been the result of vagal fatigue for example (although vagal fatigue can be ruled out in the related experiments of Martin, 1976) it could be the phenomenon reported here. An increase in heart rate beyond control (i.e.…”

Attenuation of the responses to repeated cholinergic interventions in the isolated dog atrium

“…receptor responsiveness or in ACh inactivation. Recently, we suggested that the depression of the cardiac cycle length and contractility responses to successive brief vagal nerve stimulation were due to postjunctional anechanism (Martin 1980). Gertjegerdes et d. (19'79) observed that carbachol induced an initial, rapid decline in contractile force in the isolated guinea-pig atrium.…”

High atrioventricular phase index on near-field intracardiac electrogram is associated with risk of ventricular arrhythmia

“…13 Such vagal bursts can appear at different times in successive cardiac cycles that can occur just before the AV node is excited, causing a prolongation of AV conduction. 14 It is expected that changes in atrial intervals would predict the changes and hence control ventricular intervals. This possibly explains the finding that a strong dependency of changes in subsequent ventricular intervals on atrial interval changes is associated with VT/VF outcome.…”