Abstract
To examine central sites that integrate the vagal bradycardia induced by hypoxia, heart rates were recorded continuously in spinal, precollicular, decerebrated cats during transient hypoxia induced by ventilation with 100% nitrogen. Bilateral lesions in the lateral mesencephalic reticular formation either decreased the extent of bradycardia or caused a reversal to tachycardia; anesthesia induced the same change. In contrast, bilateral lesions in the medial mesencephalic reticular formation failed to alter the bradycardia. Hence, the lateral mesencephalic reticular formation is essential for the appearance of hypoxia-induced vagal bradycardia.
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