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.
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.
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