Reeves J T, Moore L G, McCullough R E, McCullough R G, Harrison G, Tranmer B I, Micco A J, Tucker A, Weil J V
J Appl Physiol (1985). 1985 Sep;59(3):909-15. doi: 10.1152/jappl.1985.59.3.909.
The cause of headache in persons going to high altitude is unknown. Relatively severe hypoxemia in susceptible subjects could induce large increases in cerebral blood flow that then could initiate the headache. Thus we measured noninvasively, by Doppler ultrasound, changes in internal carotid arterial blood velocity (velocity) in 12 subjects in Denver (1,600 m) and repeatedly up to 7 h at a simulated altitude of 4,800 m (barometric pressure = 430 Torr). Six subjects, selected because of prior history of high-altitude headache, developed comparatively severe headache at 4,800 m, and four subjects, without such history, remained well. Two subjects developed moderate headache. Velocity at 4,800 m did not correlate with symptom development, arterial O2 saturation, or end-tidal PCO2. Also, neither velocity nor blood pressure was consistently elevated above the Denver base-line values. During measurements of hypercapnic ventilatory response in Denver, velocity increased linearly with end-tidal PCO2, confirming that our Doppler method could demonstrate an increase. Also, 30 min of isocapnic or poikilocapnic hypoxia caused small increases in velocity (+8 and +6%) during the base-line measurement at low altitude. Although even a small increase in cerebral perfusion could contribute to headache symptoms at high altitude, cerebral blood flow does not appear to play a primary role.
前往高海拔地区人群头痛的原因尚不清楚。易感人群中相对严重的低氧血症可导致脑血流量大幅增加，进而引发头痛。因此，我们采用多普勒超声对12名位于丹佛（海拔1600米）的受试者进行了无创测量，测量其颈内动脉血流速度（速度），并在模拟海拔4800米（气压 = 430托）的环境下重复测量长达7小时。6名因有高海拔头痛病史而被挑选出的受试者在4800米处出现了较为严重的头痛，4名无此类病史的受试者状况良好。2名受试者出现了中度头痛。在4800米处的速度与症状发展、动脉血氧饱和度或呼气末二氧化碳分压均无关联。此外，速度和血压均未持续高于丹佛基线值。在丹佛进行高碳酸通气反应测量期间，速度随呼气末二氧化碳分压呈线性增加，证实我们的多普勒方法能够显示出速度增加。同样，在低海拔基线测量期间，30分钟的等碳酸或变碳酸性低氧导致速度小幅增加（分别增加8%和6%）。尽管即使是脑灌注的小幅增加也可能导致高海拔地区的头痛症状，但脑血流似乎并未起主要作用。
