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1 Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT UK
2 Department of Respiratory Medicine, Leeds General Infirmary, Leeds LS1 3EX UK
3 Department of Respiratory Medicine, St James's University Hospital, Leeds LS9 7ET, UK
Asphyxia, which occurs during obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension. We have recently reported that breathing an asphyxic gas resets the baroreceptor–vascular resistance reflex towards higher pressures. The present study was designed to determine whether this effect was caused by the reduced oxygen tension, which affects mainly peripheral chemoreceptors, or by the increased carbon dioxide, which acts mainly on central chemoreceptors. We studied 11 healthy volunteer subjects aged between 20 and 55 years old (6 male). The stimulus to the carotid baroreceptors was changed using graded pressures of –40 to +60 mmHg applied to a neck chamber. Responses of vascular resistance were assessed in the forearm from changes in blood pressure (Finapres) divided by brachial blood flow velocity (Doppler) and cardiac responses from the changes in RR interval and heart rate. Stimulus–response curves were defined during (i) air breathing, (ii) hypoxia (12% O2 in N2), and (iii) hypercapnia (5% CO2 in 95% O2). Responses during air breathing were assessed both prior to and after either hypoxia or hypercapnia. We applied a sigmoid function or third order polynomial to the curves and determined the maximal differential (equivalent to peak sensitivity) and the corresponding carotid sinus pressure (equivalent to ‘set point’). Hypoxia resulted in an increase in heart rate but no significant change in mean blood pressure or vascular resistance. However, there was an increase in vascular resistance in the post-stimulus period. Hypoxia had no significant effect on baroreflex sensitivity or ‘set point’ for the control of RR interval, heart rate or mean arterial pressure. Peak sensitivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from –2.5 ± 0.4 units to –1.4 ± 0.1 units (P < 0.05) and this was restored in the post-stimulus period to –2.6 ± 0.5 units. There was no effect on ‘set point’. Hypercapnia, on the other hand, resulted in a decrease in heart rate, which remained reduced in the post-stimulus period and significantly increased mean blood pressure. Baseline vascular resistance was significantly increased and then further increased in the post-control period. Like hypoxia, hypercapnia had no effect on baroreflex control of RR interval, heart rate or mean arterial pressure. There was, also no significant change in the sensitivity of the vascular resistance responses, however, ‘set point’ was significantly increased from 74.7 ± 4 to 87.0 ± 2 mmHg (P < 0.02). This was not completely restored to pre-stimulus control levels in the post-stimulus control period (82.2 ± 3 mmHg). These results suggest that the hypoxic component of asphyxia reduces baroreceptor–vascular resistance reflex sensitivity, whilst the hypercapnic component is responsible for increasing blood pressure and reflex ‘set point’. Hypercapnia appears to have a lasting effect after the removal of the stimulus. Thus the effect of both peripheral and central chemoreceptors on baroreflex function may contribute to promoting hypertension in patients with obstructive sleep apnoea.
(Received 5 July 2005;
accepted after revision 12 August 2005;
first published online 18 August 2005)
Corresponding author V. Cooper: Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK. Email: mrpvlw{at}leeds.ac.uk
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