This preclinical study demonstrates that hypoxia-induced bradycardia in cats is primarily a reflex response mediated by afferent vagal fibers from ventricular receptors.
Hypoxia-induced bradycardia may be reflex-mediated via ventricular receptors in cats; leaves open translation to human physiology and clinical relevance.
In chloralose anesthetized cats blood pressure, heart rate and left ventricular pressure were measured as well as changes in ventricular volume by means of a cardiometer. Hypoxia was induced by ventilating the animal with a gas mixture containing 3 % O 2 . 1–2 min after the onset of hypoxia cardiac volume started to increase and simultaneously a bradycardia developed. The bradycardia was eliminated by vagal cooling indicating that it was elicited by nervous mechanisms rather than by local myocardial factors. After injection of procaine (0,3–0,5 %) into the cardiometer the afferent vagal fibres from the ventricles could be blocked, leaving the efferent fibres to the sinus node intact. Such selective denervation of the ventricular receptors markedly reduced the bradycardia during hypoxia, suggesting that it is mainly a reflex response emanating from ventricular receptors.
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Peter Thorén (1973) studied this question.
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