Why the study?
Does acute hypoxia alter heart rate, arterial pressure, cardiac output, and ventilation in unanesthetized rabbits?
Does acute hypoxia alter heart rate, arterial pressure, cardiac output, and ventilation in unanesthetized rabbits?
Acute hypoxia in unanesthetized rabbits triggers a reflex bradycardia and systemic vasoconstriction mediated by carotid chemoreceptors and baroreceptors.
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Animal data on vagal hypoxic bradycardia in rabbits may guide mechanistic studies; leaves open human translation.
The circulatory and respiratory changes occurring during the first 5 min. of hypoxia were studied in unanæsthetized rabbits. Mild degrees of hypoxia produced an increase in ventilation in the rabbit, without eliciting a detectable circulatory response. The early circulatory effects consisted of bradycardia, a rise in mean arterial pressure and a fall in cardiac output, indicating predominant systemic vasoconstriction. The magnitude of the bradycardia and rise in arterial pressure were related to the fall in arterial O 2 saturation. Atropine or vagotomy reduced or abolished the bradycardia, but greatly accentuated the rise in blood pressure. Denervation of the carotid baroreceptors and chemoreceptors almost abolished the bradycardia and diminished the rise in blood pressure.
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Korner et al. (1960) studied this question.
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