Short-term intermittent hypoxia leads to sustained sympathetic activation and a small increase in blood pressure in healthy humans. Because obstructive sleep apnea, a condition associated with intermittent hypoxia, is accompanied by elevated sympathetic activity and enhanced sympathetic chemoreflex responses to acute hypoxia, we sought to determine whether intermittent hypoxia also enhances chemoreflex activity in healthy humans. To this end, we measured the responses of muscle sympathetic nerve activity (MSNA, peroneal microneurography) to arterial chemoreflex stimulation and deactivation before and following exposure to a paradigm of repetitive hypoxic apnea (20 s/min for 30 min; O(2) saturation nadir 81.4 +/- 0.9%). Compared with baseline, repetitive hypoxic apnea increased MSNA from 113 +/- 11 to 159 +/- 21 units/min (P = 0.001) and mean blood pressure from 92.1 +/- 2.9 to 95.5 +/- 2.9 mmHg (P = 0.01; n = 19). Furthermore, compared with before, following intermittent hypoxia the MSNA (units/min) responses to acute hypoxia [fraction of inspired O(2) (Fi(O(2))) 0.1, for 5 min] were enhanced (pre- vs. post-intermittent hypoxia: +16 +/- 4 vs. +49 +/- 10%; P = 0.02; n = 11), whereas the responses to hyperoxia (Fi(O(2)) 0.5, for 5 min) were not changed significantly (P = NS; n = 8). Thus 30 min of intermittent hypoxia is capable of increasing sympathetic activity and sensitizing the sympathetic reflex responses to hypoxia in normal humans. Enhanced sympathetic chemoreflex activity induced by intermittent hypoxia may contribute to altered neurocirculatory control and adverse cardiovascular consequences in sleep apnea.
The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O(2) fraction = 0.1) before and after regional sympathetic blockade with the alpha-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with alpha- receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 +/- 0.05 vs. 1.03 +/- 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 +/- 0.14 vs. 0.53 +/- 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 +/- 75 vs. 826 +/- 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 +/- 66 vs. 661 +/- 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 +/- 0.06 vs. 1.16 +/- 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 +/- 0.16 vs. 0.87 +/- 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O(2) saturation = 77 +/- 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.
Increased TR following CRMD implantation is relatively common (33%) and correlated with subsequent risk of hospitalization for heart failure. A preventive strategy and close monitoring for development or worsening of CHF after CRMD implantation may help prevent hospital admissions.
In healthy humans, short‐term intermittent hypoxia (IH) raises sympathetic nerve activity mirroring the sympathetic activation seen in patients with obstructive sleep apnea. To explore the role of oxidative stress, we measured blood pressure (BP), sympathetic activity (microneurography) and flow‐mediated brachial artery dilation before and following IH (30 episodes, O2 saturation nadir ~82%) with and without the antioxidant ascorbic acid (50 mg/kg iv) in healthy subjects (age 26±1 yrs; n=13). During saline infusion, IH produced a sustained increase in sympathetic activity (pre vs. post 20.0±1.8 vs. 25.2±1.8 bursts/min; P<0.05) and a small rise of mean BP (pre vs. post 86±2 vs. 89±3 mmHg; P<0.05). In contrast, on a separate day during infusion of ascorbic acid, IH did not raise sympathetic activity (pre vs. post 20.2±2.1 vs. 20.5±2.6 bursts/min; P=NS) or BP (pre vs. post 88±2 vs. 89±2 mmHg; P=NS). Moreover, whereas during saline infusion IH reduced flow‐mediated dilation (pre vs. post 6.8±1.3 vs. 3.2±1.6%; P<0.05), with ascorbic acid this effect was not seen (pre vs. post 6.0±1.2 vs. 6.1±1.4%; P=NS, n=8). These data suggest indirectly that oxidative stress may play a role in the sympathetic activation and vascular dysfunction induced by IH.Supported by P01 HL077670 and UL1 RR033184.
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