Abstract
Cerebral blood flow (CBF) is significantly influenced by exposure to hypoxia, both hypobaric and normobaric. Alterations in cerebral blood flow can play a crucial role in the pathogenesis of acute mountain sickness (AMS) and its symptoms, especially headache, dizziness, and nausea. Acupuncture has been proven to be effective in treating some cerebrovascular disorders and PC6 Nei Guan stimulation seems to enhance cerebral blood flow. Therefore, we have hypothesized that PC6 Nei Guan stimulation could affect CBF in acute hypoxia and could be used to contrast AMS symptoms. We evaluated blood flow in the middle cerebral artery (MCA) in normoxia, after 15 min in normobaric hypoxia (fraction of inspired oxygen (FiO2) 14%, corresponding to 3600 m a.s.l.) in basal conditions, and after PC6 Nei Guan stimulation, both by needle and by pressure. No comparisons with other acupuncture points and sham acupuncture were done. PC6 stimulation seemed to counteract the effects of acute normobaric hypoxia on end-diastolic velocity (EDV) in MCA, especially after acupuncture, and significantly reduced systolic and diastolic blood pressure. A rebalance of CBF could control some AMS symptoms, but further studies are necessary.
Highlights
phase tract of the systolic velocity (PSV) and end-diastolic velocity (EDV) after hypoxia seemed to increase more in the control group, whereas for the other indices under examination, there were no differences in the measurements at the three time points (Table 2 and Figures 5–8)
Through multilevel mixed-effects linear regression, we evaluated Cerebral blood flow (CBF) in middle cerebral artery (MCA) in normoxia, and after 5 and 15 min in normobaric hypoxia (FiO2 14% corresponding to 3600 m a.s.l.), in the control group and after PC6 stimulation
In all the subjects recruited, acute normobaric hypoxia caused a significant increase in PSV and EDV, and a reduction in pulsatility index (PI) and resistive index (RI)—in agreement with the data of Bian
Summary
CBF regulation is a complex mechanism, significantly influenced by exposure to high altitude hypoxia. It is well documented that CBF increases in response to the severity of hypoxic stimuli in humans via cerebral vasodilation [2,3,4]. As observed by Berré, breathing a hypoxic mixture (i.e., with FiO2 equal to 12.5%) for fifteen minutes causes an increase in flow velocity in the middle cerebral artery (MCA), both in subjects with a history of pulmonary oedema at high altitudes, in normal controls, and in elite climbers who tolerate high altitudes well [5]. Baumgartner found that the flow velocity in the MCA, after a rapid climb to 4559 m, increased significantly over the twenty-four hours, and remained elevated for fortyeight hours. The increase was higher in subjects with symptoms of acute mountain sickness than in asymptomatic volunteers and was directly correlated with arterial PO2 [6]
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