Tarasiuk A, Scharf S M
Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New Hyde Park, NY 11042, USA.
J Basic Clin Physiol Pharmacol. 1994 Jul-Dec;5(3-4):253-68. doi: 10.1515/jbcpp.1994.5.3-4.253.
We recently reported that during simulated central apneas (SCA) heart frequency was more severely depressed than during obstructive apneas. In the present study, we examined factors influencing this response including hypoxia, hypercapnia, mechanoreceptor input and the role of the vagus nerve. In 11 paralyzed and mechanically ventilated animals, SCA was produced by turning the ventilator off for 1 min and on for 1 min. This was done with and without hypoxia, before and after bilateral cervical vagotomy. We also compared the effects of SCA with matched intermittent hypoxia. Under all conditions during room air breathing arterial pO2 fell and pCO2 rose to approximately the same values: 49 and 57 torr, respectively. Compared with baseline, during SCA following room air breathing blood pressure and cardiac output did not change significantly, and heart frequency decreased by 47% (p<0.001). Following 100% O2 breathing, during SCA mean blood pressure did not change, cardiac output decreased by 20% (p<0.05) and heart frequency decreased by 27% (p<0.02), a decrease which was significantly less than that following room air breathing (p<0.02). Immediately upon resuming ventilation, on room air, heart frequency increased by 15 bpm (p<0.02); heart frequency did not increase post-apnea an 100% O2. After vagotomy, following room air breathing, blood pressure increased during apnea by 32% (p<0.001) and heart frequency decreased by only 10% (p<0.05). Oxygen breathing prevented the increase in blood pressure during apnea but heart frequency was still reduced by 16% (p<0.05). During intermittent hypoxia matched for periodicity and pO2 to SCA, there were no changes in heart frequency. We conclude that the cardiovascular response to apnea is more than just that to intermittent hypoxia, and is critically dependent on loss of respiratory mechanoreceptor afferent input, hypercapnia, and an intact vagus nerve. Blood pressure responses are also dependent on the vagus nerve.
