Systemic blood pressure, arterial stiffness and pulse waveform analysis at altitude.

OBJECTIVES: Systemic arterial pressure rises on acute exposure to high altitude and changes in blood pressure (BP) and endothelial function may be important in the pathogenesis of clinical syndromes occurring at high altitude. METHODS: Arterial BP, stiffness (SI) and tone (RI) were studied over 11 days in 17 subjects (three having mild hypertension) ascending to 3,450m and 4,770m using a non-invasive, finger photoplethysmography technique. RESULTS: At 3,450m BP rose from mean 131/75 mmHg (SD 23/12) to 145/86 (23/12) and was maintained at this level (p < 0.001). SI did not change significantly from 8.5 m/sec (2.5) to 9.7 (3.2). RI fell during the first day at 3,450m from 74.4% (7.9) to 70.5% (13.8) (NS p > 0.05) and to 69.9% (12.0) (p < 0.02) at 4,770m but then reverted to baseline. Changes in SI and RI did not relate to changes in blood pressure. Changes in both arterial stiffness and tone were similar in those who developed AMS compared with those who did not. Baseline SI tended to be higher in the three subjects with hypertension 11.1m/sec (SD 2.7)) compared with the normotensives 8.3 m/sec (SD 2.7) (NS) and baseline RI lower 74.7% (7.0) compared with the normotensives 76.5% (8.5) (NS). Changes in SI and RI at altitude in the hypertensive subjects were similar to the non-hypertensive subjects. CONCLUSIONS: We conclude that acute exposure temporarily affected endothelial function as measured by a change in vascular tone but this did not predict the development of AMS. The rise in arterial BP was not related to changes in arterial stiffness or tone.

Altered free radical metabolism in acute mountain sickness: implications for dynamic cerebral autoregulation and blood-brain barrier function.

We tested the hypothesis that dynamic cerebral autoregulation (CA) and blood-brain barrier (BBB) function would be compromised in acute mountain sickness (AMS) subsequent to a hypoxia-mediated alteration in systemic free radical metabolism. Eighteen male lowlanders were examined in normoxia (21% O(2)) and following 6 h passive exposure to hypoxia (12% O(2)). Blood flow velocity in the middle cerebral artery (MCAv) and mean arterial blood pressure (MAP) were measured for determination of CA following calculation of transfer function analysis and rate of regulation (RoR). Nine subjects developed clinical AMS (AMS+) and were more hypoxaemic relative to subjects without AMS (AMS-). A more marked increase in the venous concentration of the ascorbate radical (A(*-)), lipid hydroperoxides (LOOH) and increased susceptibility of low-density lipoprotein (LDL) to oxidation was observed during hypoxia in AMS+ (P < 0.05 versus AMS-). Despite a general decline in total nitric oxide (NO) in hypoxia (P < 0.05 versus normoxia), the normoxic baseline plasma and red blood cell (RBC) NO metabolite pool was lower in AMS+ with normalization observed during hypoxia (P < 0.05 versus AMS-). CA was selectively impaired in AMS+ as indicated both by an increase in the low-frequency (0.07-0.20 Hz) transfer function gain and decrease in RoR (P < 0.05 versus AMS-). However, there was no evidence for cerebral hyper-perfusion, BBB disruption or neuronal-parenchymal damage as indicated by a lack of change in MCAv, S100beta and neuron-specific enolase. In conclusion, these findings suggest that AMS is associated with altered redox homeostasis and disordered CA independent of barrier disruption.