Transcerebral exchange kinetics of nitrite and calcitonin gene-related peptide in acute mountain sickness: evidence against trigeminovascular activation?

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

SN - 0039-2499

VL - 40

SP - 2205

EP - 2208

JO - Stroke

JF - Stroke

IS - 6

ER -