Dominic S. Puleo

Baroreflex-induced sympathetic activation does not alter cerebrovascular CO2 responsiveness in humans

We investigated the effect of baroreflex‐induced sympathetic activation, produced by lower body negative pressure (LBNP) at −40 mmHg, on cerebrovascular responsiveness to hyper‐ and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end‐tidal carbon dioxide pressure (PET,CO2) of +10, +5, 0, −5, and −10 mmHg relative to eupnoea. The slopes of the linear relationships between PET,CO2 and CFV were computed separately for hyper‐ and hypocapnia during the LBNP and no‐LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 ± 2 mmHg decrease in PET,CO2, which was corrected by CO2 supplementation of the inspired air. LBNP did not affect cerebrovascular CO2 response slopes during steady‐state hypercapnia (3.14 ± 0.24 vs. 2.96 ± 0.26 cm s−1 mmHg−1) or hypocapnia (1.31 ± 0.18 vs. 1.32 ± 0.19 cm s−1 mmHg−1), or the CFV responses to voluntary apnoea (+51 ± 19 vs.+50 ± 18 %). Thus, cerebrovascular CO2 responsiveness was not altered by baroreflex‐induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO2 pressure.

Arousal from sleep shortens sympathetic burst latency in humans

1 Bursts of sympathetic activity in muscle nerves are phase‐locked to the cardiac cycle by the sinoaortic baroreflexes. Acoustic arousal from non‐rapid eye movement (NREM) sleep reduces the normally invariant interval between the R‐wave of the electrocardiogram (ECG) and the peak of the corresponding sympathetic burst; however, the effects of other forms of sleep disruption (i.e. spontaneous arousals and apnoea‐induced arousals) on this temporal relationship are unknown. 2 We simultaneously recorded muscle sympathetic nerve activity in the peroneal nerve (intraneural electrodes) and the ECG (surface electrodes) in seven healthy humans and three patients with sleep apnoea syndrome during NREM sleep. 3 In seven subjects, burst latencies were shortened subsequent to spontaneous K complexes (1.297 ± 0.024 s, mean ± s.e.m.) and spontaneous arousals (1.268 ± 0.044 s) compared with latencies during periods of stable NREM sleep (1.369 ± 0.023 s). In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 ± 0.038 vs. 1.342 ± 0.026 s); however, following apnoea‐induced EEG perturbations, burst latencies were reduced (1.214 ± 0.034 s). 4 Arousal‐induced reduction in sympathetic burst latency may reflect a temporary diminution of baroreflex buffering of sympathetic outflow. If so, the magnitude of arterial pressure perturbations during sleep (e.g. those caused by sleep disordered breathing and periodic leg movements) may be augmented by arousal.