Transcerebral exchange kinetics of nitrite and calcitonin gene-related peptide in acute mountain sickness: evidence against trigeminovascular activation?
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Transcerebral exchange kinetics of nitrite and calcitonin gene-related peptide in acute mountain sickness: evidence against trigeminovascular activation? / Bailey, Damian M; Taudorf, Sarah; Berg, Ronan M G; Jensen, Lars T; Lundby, Carsten; Evans, Kevin A; James, Philip E; Pedersen, Bente K; Moller, Kirsten.
I: Stroke, Bind 40, Nr. 6, 2009, s. 2205-8.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Transcerebral exchange kinetics of nitrite and calcitonin gene-related peptide in acute mountain sickness: evidence against trigeminovascular activation?
AU - Bailey, Damian M
AU - Taudorf, Sarah
AU - Berg, Ronan M G
AU - Jensen, Lars T
AU - Lundby, Carsten
AU - Evans, Kevin A
AU - James, Philip E
AU - Pedersen, Bente K
AU - Moller, Kirsten
N1 - Keywords: Adult; Altitude Sickness; Anoxia; Brain Chemistry; Calcitonin Gene-Related Peptide; Cerebrovascular Circulation; Headache; Humans; Kinetics; Luminescence; Male; Nitric Oxide; Questionnaires; Trigeminal Nerve
PY - 2009
Y1 - 2009
N2 - BACKGROUND AND PURPOSE: High-altitude headache is the primary symptom associated with acute mountain sickness, which may be caused by nitric oxide-mediated activation of the trigeminovascular system. Therefore, the present study examined the effects of inspiratory hypoxia on the transcerebral exchange kinetics of the vasoactive molecules, nitrite (NO(2)(*)), and calcitonin gene-related peptide (CGRP). METHODS: Ten males were examined in normoxia and after 9-hour exposure to hypoxia (12.9% O(2)). Global cerebral blood flow was measured by the Kety-Schmidt technique with paired samples obtained from the radial artery and jugular venous bulb. Plasma CGRP and NO(2)(*) were analyzed via radioimmunoassay and ozone-based chemiluminescence. Net cerebral exchange was calculated by the Fick principle and acute mountain sickness/headache scores assessed via clinically validated questionnaires. RESULTS: Hypoxia increased cerebral blood flow with a corresponding increase in acute mountain sickness and headache scores (P<0.05 vs normoxia). Hypoxia blunted the cerebral uptake of NO(2)(*), whereas CGRP exchange remained unaltered. No relationships were observed between the change (hypoxia-normoxia) in cerebral NO(2)(*) or CGRP exchange and acute mountain sickness/headache scores (P>0.05). CONCLUSIONS: These findings argue against sustained trigeminovascular system activation as a significant event in acute mountain sickness.
AB - BACKGROUND AND PURPOSE: High-altitude headache is the primary symptom associated with acute mountain sickness, which may be caused by nitric oxide-mediated activation of the trigeminovascular system. Therefore, the present study examined the effects of inspiratory hypoxia on the transcerebral exchange kinetics of the vasoactive molecules, nitrite (NO(2)(*)), and calcitonin gene-related peptide (CGRP). METHODS: Ten males were examined in normoxia and after 9-hour exposure to hypoxia (12.9% O(2)). Global cerebral blood flow was measured by the Kety-Schmidt technique with paired samples obtained from the radial artery and jugular venous bulb. Plasma CGRP and NO(2)(*) were analyzed via radioimmunoassay and ozone-based chemiluminescence. Net cerebral exchange was calculated by the Fick principle and acute mountain sickness/headache scores assessed via clinically validated questionnaires. RESULTS: Hypoxia increased cerebral blood flow with a corresponding increase in acute mountain sickness and headache scores (P<0.05 vs normoxia). Hypoxia blunted the cerebral uptake of NO(2)(*), whereas CGRP exchange remained unaltered. No relationships were observed between the change (hypoxia-normoxia) in cerebral NO(2)(*) or CGRP exchange and acute mountain sickness/headache scores (P>0.05). CONCLUSIONS: These findings argue against sustained trigeminovascular system activation as a significant event in acute mountain sickness.
U2 - 10.1161/STROKEAHA.108.543959
DO - 10.1161/STROKEAHA.108.543959
M3 - Journal article
C2 - 19359638
VL - 40
SP - 2205
EP - 2208
JO - Stroke
JF - Stroke
SN - 0039-2499
IS - 6
ER -
ID: 20008997