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. 2007 Jul;23(9):721-6.
doi: 10.1016/s0828-282x(07)70817-6.

Mechanism of hypotensive transients associated with abrupt bradycardias in conscious rabbits

Robert S Sheldon  1 , Christopher I Wright, Henry J Duff, Ela Thakore, Anne M Gillis, Daniel E Roach
Affiliations

Mechanism of hypotensive transients associated with abrupt bradycardias in conscious rabbits

Robert S Sheldon et al. Can J Cardiol. 2007 Jul.

Abstract
in English, French

Background: Transient bradycardic hypotensive events occur in resting rabbits. If the hypotension is due to vasodepression, these events may be a model for vasovagal syncope.

Objectives: To determine whether these events are responses to brief stimuli and whether the hypotensive episodes are solely due to rapid-onset bradycardia.

Methods: Rabbits were instrumented with subcutaneous electrocardiogram leads, and cannulae were acutely inserted into an ear artery to obtain continuous arterial pressure measurements. Exposure to brief, low-level auditory stimuli at 5 kHz transiently increased the RR interval by approximately 70 ms and decreased mean arterial pressure by approximately 5 mmHg.

Results: These evoked bradycardic hypotensive events were almost identical to previously reported spontaneous bradycardic hypotensive events. Intra-aortic telemetric blood pressure monitoring was used to demonstrate that the evoked hypotension reflected prolonged diastole, rather than local ear arterial vasoconstriction. Furthermore, administration of the muscarinic blocker glycopyrrolate abolished not only bradycardia (RR interval 64+/-14 ms to 1+/-1 ms; P<0.0001), but also hypotension (--4.1+/-0.8 mmHg to --0.4+/-0.3 mmHg; P=0.0055). Finally, cardiac pacing abolished the inducible bradycardia (RR interval 51+/-10 ms to 2+/-1 ms; P=0.0006) and its associated hypotension (--4.1+/-0.7 mmHg to --1.2+/-0.3 mmHg; P=0.003).

Conclusions: Brief auditory stimuli evoked a transient bradycardia mediated by cardiac muscarinic receptors and consequent hypotension. This is not a model for vasovagal syncope.

CONTEXTE:: Les lapins au repos connaissent des épisodes d’hypotension transitoire, associée à de la bradycardie. Si l’hypotension est due à un collapsus circulatoire, les épisodes pourraient servir de modèle de syncope vasovagale.

BUT:: L’étude avait pour but de déterminer si les chutes de pression étaient des réactions à de brefs stimulus ou si les épisodes d’hypotension étaient tout simplement dus à l’apparition soudaine de bradycardie.

MÉTHODE:: On a posé, sur des lapins, des électrodes sous-cutanées à électrocardiogramme, et des canules ont été placées très précisément dans une artère auriculaire pour fournir des mesures continues de la pression artérielle. Une exposition à de brefs stimulus auditifs de faible intensité à une fréquence de 5 kHz a eu pour effet d’allonger temporairement l’intervalle RR d’environ 70 ms et de réduire la pression artérielle moyenne d’environ 5 mm Hg.

RÉSULTATS:: Ces épisodes provoqués d’hypotension d’origine bradycardique étaient presque identiques aux épisodes spontanés d’hypotension d’origine bradycardique, mentionnés précédemment. Un appareil intra-aortique de mesure télémétrique de la pression artérielle a montré que l’hypotension provoquée résultait d’une diastole prolongée plutôt que d’une vasoconstriction locale de l’artère auriculaire. De plus, l’administration de glycopyrrolate, un inhibiteur muscarinique, a supprimé non seulement la bradycardie (intervalle RR : 64±14 ms à 1±1 ms; p < 0,0001), mais aussi l’hypotension (−4,1±0,8 mm Hg à −0,4±0,3 mm Hg; p = 0,0055). Enfin, la stimulation cardiaque a mis fin à la bradycardie provoquée (intervalle RR : 51±10 ms à 2±1 ms; p = 0,0006) et à l’hypotension associée (−4,1±0,7 mm Hg à −1,2±0,3 mm Hg; p = 0,003).

CONCLUSIONS:: Les brefs stimulus auditifs ont provoqué de la bradycardie transitoire, médiée par les récepteurs muscariniques du cœur, et il s’en est suivi de l’hypotension. Aussi ne s’agit-il pas d’un modèle de syncope vasovagale.

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Figures

Figure 1)
Figure 1)
An example of traces showing auditory evoked responses in one animal. Traces shown are electrocardiogram (ECG), RR interval, ear arterial blood pressure and mean ear arterial pressure. The stimulus is marked on the top line
Figure 2)
Figure 2)
Comparison of spontaneous and induced events. These are group-averaged signals comparing induced RR intervals and MAP responses (left) with spontaneous bradycardic hypotensive events (right). The magnitudes and shapes of these events are almost identical. Data are presented as mean of all means on a per-animal basis and are taken from a total of 21 animals (10 induced, 11 spontaneous [16]). No difference was found between the magnitude of the RR interval and mean arterial blood pressure events (P>0.05, Student’s unpaired t test). Refer to Table 1 for quantitative comparison of size and shape parameters
Figure 3)
Figure 3)
Comparison of intra-aortic and central ear artery blood pressure recordings during induced bradycardic hypotension. Continuous and simultaneous blood pressure recordings during auditory stimuli (top). Correlation of beat-to-beat changes in blood pressure using the two techniques for each of the three rabbit experiments (bottom). MAP Mean arterial blood pressure
Figure 4)
Figure 4)
Correlation of maximal RR interval (RR) and mean arterial blood pressure (MAP) changes in the 30 induction attempts in six rabbits under control conditions (left). Correlation of beat-to-beat changes in RR and MAP for three rabbits during representative bradycardic hypotensive events (right). Δ Change
Figure 5)
Figure 5)
An example of responses in one animal under control conditions (top left) and with glycopyrrolate (bottom left). Traces shown are of electrocardiogram (ECG), RR interval (RR), arterial blood pressure (BP) and mean arterial BP (MAP). An example of responses in one animal under control conditions (top right) and with pacing (bottom right). Traces shown are of ECG, RR, arterial BP and MAP. The auditory stimulus is marked with the vertical stippled bar
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