Abstract
The role of prostaglandins in the pathogenesis of acute mountain sickness and two hypoxia-induced vascular responses was evaluated using the cyclooxygenase inhibitor naproxen. Eleven men spent 24 hours at sea level, followed by 34 hours of decompression to 428 mm Hg while receiving naproxen (N), 250 mg twice daily or placebo (P) in a double-blind crossover trial. Serum naproxen levels measured by high pressure liquid chromatography were changed by hypoxia. The severity of acute mountain sickness (AMS) by the Environmental Symptom Questionnaire scores and observer assessment were unaffected by drug treatment. Retinal artery diameter measured from projected fundus photographs was increased after 27 hours at altitude (11.4 ± .5 mm) vs. sea level (9.4 ± .5 mm, p < 0.05) during both trials. Upright mean arterial pressure fell after 6 hours at altitude (79 ± 3 mm Hg during N and P vs. 92 ± 3 at sea level, p < 0.01). Minute ventilation, end expiratory alveolar PO2 and PCO2 did not differ between drug trials. This study suggests vasodilating prostaglandins do not have a major role in the genesis of AMS, hypoxia-induced retinal vasodilatation, or postural blood pressure responses in man.
| Original language | English |
|---|---|
| Pages (from-to) | 15-20 |
| Number of pages | 6 |
| Journal | American Journal of the Medical Sciences |
| Volume | 292 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1 Jan 1986 |
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The effect of naproxen on acute mountain sickness and vascular responses to hypoxia. / Meehan, R. T.; Cymerman, A.; Rock, P.; Fulco, C. S.; Hoffman, J.; Abernathy, C.; Needleman, S.; Maher, J. T.
In: American Journal of the Medical Sciences, Vol. 292, No. 1, 01.01.1986, p. 15-20.Research output: Contribution to journal › Article
TY - JOUR
T1 - The effect of naproxen on acute mountain sickness and vascular responses to hypoxia
AU - Meehan, R. T.
AU - Cymerman, A.
AU - Rock, P.
AU - Fulco, C. S.
AU - Hoffman, J.
AU - Abernathy, C.
AU - Needleman, S.
AU - Maher, J. T.
PY - 1986/1/1
Y1 - 1986/1/1
N2 - The role of prostaglandins in the pathogenesis of acute mountain sickness and two hypoxia-induced vascular responses was evaluated using the cyclooxygenase inhibitor naproxen. Eleven men spent 24 hours at sea level, followed by 34 hours of decompression to 428 mm Hg while receiving naproxen (N), 250 mg twice daily or placebo (P) in a double-blind crossover trial. Serum naproxen levels measured by high pressure liquid chromatography were changed by hypoxia. The severity of acute mountain sickness (AMS) by the Environmental Symptom Questionnaire scores and observer assessment were unaffected by drug treatment. Retinal artery diameter measured from projected fundus photographs was increased after 27 hours at altitude (11.4 ± .5 mm) vs. sea level (9.4 ± .5 mm, p < 0.05) during both trials. Upright mean arterial pressure fell after 6 hours at altitude (79 ± 3 mm Hg during N and P vs. 92 ± 3 at sea level, p < 0.01). Minute ventilation, end expiratory alveolar PO2 and PCO2 did not differ between drug trials. This study suggests vasodilating prostaglandins do not have a major role in the genesis of AMS, hypoxia-induced retinal vasodilatation, or postural blood pressure responses in man.
AB - The role of prostaglandins in the pathogenesis of acute mountain sickness and two hypoxia-induced vascular responses was evaluated using the cyclooxygenase inhibitor naproxen. Eleven men spent 24 hours at sea level, followed by 34 hours of decompression to 428 mm Hg while receiving naproxen (N), 250 mg twice daily or placebo (P) in a double-blind crossover trial. Serum naproxen levels measured by high pressure liquid chromatography were changed by hypoxia. The severity of acute mountain sickness (AMS) by the Environmental Symptom Questionnaire scores and observer assessment were unaffected by drug treatment. Retinal artery diameter measured from projected fundus photographs was increased after 27 hours at altitude (11.4 ± .5 mm) vs. sea level (9.4 ± .5 mm, p < 0.05) during both trials. Upright mean arterial pressure fell after 6 hours at altitude (79 ± 3 mm Hg during N and P vs. 92 ± 3 at sea level, p < 0.01). Minute ventilation, end expiratory alveolar PO2 and PCO2 did not differ between drug trials. This study suggests vasodilating prostaglandins do not have a major role in the genesis of AMS, hypoxia-induced retinal vasodilatation, or postural blood pressure responses in man.
UR - http://www.scopus.com/inward/record.url?scp=0022916679&partnerID=8YFLogxK
U2 - 10.1097/00000441-198607000-00003
DO - 10.1097/00000441-198607000-00003
M3 - Article
C2 - 3521277
AN - SCOPUS:0022916679
VL - 292
SP - 15
EP - 20
JO - American Journal of the Medical Sciences
JF - American Journal of the Medical Sciences
SN - 0002-9629
IS - 1
ER -