We investigated the role of the autonomic nervous system to cardiovascular responses to obstructive
apnea in awake, unrestrained rats, and measured expression of Fos induced by
apnea in the brainstem. We implanted a tracheal balloon contained in a rigid tube to allow the induction of
apnea without inducing
pain in the trachea. During bouts of 15s of
apnea, heart rate fell from 371±8 to 161±11bpm (mean±SEM, n=15, p<0.01) and arterial pressure increased from 115±2 to 131±4mmHg (p<0.01).
Bradycardia was due to parasympathetic activity because it was blocked by the
muscarinic antagonist,
methylatropine. The pressor response was due to vasoconstriction caused by sympathetic activation because it was blocked by the α1 antagonist,
prazosin.
Apnea induced Fos expression in several brainstem areas involved in cardiorespiratory control such as the nucleus of the solitary tract (NTS), ventrolateral medulla (VLM), and pons.
Ligation of the carotid body artery reduced
apnea-induced
bradycardia, blocked heart rate responses to i.v. injection of
cyanide, reduced Fos expression in the caudal NTS, and increased Fos expression in the rostral VLM. In conclusion,
apnea activates neurons in regions that process signals from baroreceptors, chemoreceptors, pulmonary receptors, and regions responsible for autonomic and respiratory activity both in the presence and absence of carotid chemoreceptors.