Background and Purpose-Impaired cerebral autoregulation (CA) from high-altitude hypoxia may cause high-altitude cerebral edema in newcomers to a higher altitude. Furthermore, it is assumed that high-altitude natives have preserved CA. However, cerebral autoregulation has not been studied at altitude. Methods-We studied CA in 10 subjects at sea level and in 9 Sherpas and 10 newcomers at an altitude of 4243 m by evaluating the effect of an increase of mean arterial blood pressure (MABP) with phenylephrine infusion on the blood flow velocity in the middle cerebral artery (Vmca), using transcranial Doppler. Theoretically, no change of Vmca in response to an increase in MABP would imply perfect autoregulation. Complete loss of autoregulation is present if Vmca changes proportionally with changes of MABP. Results-In the sea-level group, at a relative MABP increase of 23Ϯ4% during phenylephrine infusion, relative Vmca did not change essentially from baseline Vmca (2Ϯ7%, Pϭ0.36), which indicated intact autoregulation. In the Sherpa group, at a relative MABP increase of 29Ϯ7%, there was a uniform and significant increase of Vmca of 24Ϯ9% (PϽ0.0001) from baseline Vmca, which indicated loss of autoregulation. The newcomers showed large variations of Vmca in response to a relative MABP increase of 21Ϯ6%. Five subjects showed increases of Vmca of 22% to 35%, and 2 subjects showed decreases of Vmca of 21% and 23%. Conclusions-All Sherpas and the majority of the newcomers showed impaired CA. It indicates that an intact autoregulatory response to changes in blood pressure is probably not a hallmark of the normal human cerebral vasculature at altitude and that impaired CA does not play a major role in the occurrence of cerebral edema in newcomers to the altitude.

The purpose of this study was twofold: 1) to determine whether at high altitude cerebral blood flow (CBF) as assessed during CO2 inhalation and during hyperventilation in subjects with acute mountain sickness (AMS) was different from that in subjects without AMS and 2) to compare the CBF as assessed under similar conditions in Sherpas at high altitude and in subjects at sea level. Resting control values of blood flow velocity in the middle cerebral artery (VMCA), pulse oxygen saturation (SaO2), and transcutaneous PCO2 were measured at 4,243 m in 43 subjects without AMS, 17 subjects with AMS, 20 Sherpas, and 13 subjects at sea level. Responses of CO2 inhalation and hyperventilation on VMCA, SaO2, and transcutaneous PCO2 were measured, and the cerebral vasomotor reactivity (VMR = DeltaVMCA/PCO2) was calculated as the fractional change of VMCA per Torr change of PCO2, yielding a hypercapnic VMR and a hypocapnic VMR. AMS subjects showed a significantly higher resting control VMCA than did no-AMS subjects (74 +/- 22 and 56 +/- 14 cm/s, respectively; P < 0.001), and SaO2 was significantly lower (80 +/- 8 and 88 +/- 3%, respectively; P < 0.001). Resting control VMCA values in the sea-level group (60 +/- 15 cm/s), in the no-AMS group, and in Sherpas (59 +/- 13 cm/s) were not different. Hypercapnic VMR values in AMS subjects were 4.0 +/- 4.4, in no-AMS subjects were 5.5 +/- 4. 3, in Sherpas were 5.6 +/- 4.1, and in sea-level subjects were 5.6 +/- 2.5 (not significant). Hypocapnic VMR values were significantly higher in AMS subjects (5.9 +/- 1.5) compared with no-AMS subjects (4.8 +/- 1.4; P < 0.005) but were not significantly different between Sherpas (3.8 +/- 1.1) and the sea-level group (2.8 +/- 0.7). We conclude that AMS subjects have greater cerebral hemodynamic responses to hyperventilation, higher VMCA resting control values, and lower SaO2 compared with no-AMS subjects. Sherpas showed a cerebral hemodynamic pattern similar to that of normal subjects at sea level.

Cerebral autoregulation is impaired in Himalayan high-altitude residents who live above 4,200 m. This study was undertaken to determine the altitude at which this impairment of autoregulation occurs. A second aim of the study was to test the hypothesis that administration of oxygen can reverse this impairment in autoregulation at high altitudes. In four groups of 10 Himalayan high-altitude dwellers residing at 1,330, 2,650, 3,440, and 4,243 m, arterial oxygen saturation (Sa(O(2))), blood pressure, and middle cerebral artery blood velocity were monitored during infusion of phenylephrine to determine static cerebral autoregulation. On the basis of these measurements, the cerebral autoregulation index (AI) was calculated. Normally, AI is between zero and 1. AI of 0 implies absent autoregulation, and AI of 1 implies intact autoregulation. At 1,330 m (Sa(O(2)) = 97%), 2,650 m (Sa(O(2)) = 96%), and 3,440 m (Sa(O(2)) = 93%), AI values (mean +/- SD) were, respectively, 0.63 +/- 0.27, 0.57 +/- 0.22, and 0.57 +/- 0.15. At 4,243 m (Sa(O(2)) = 88%), AI was 0.22 +/- 0.18 (P < 0.0005, compared with AI at the lower altitudes) and increased to 0.49 +/- 0.23 (P = 0.008, paired t-test) when oxygen was administered (Sa(O(2)) = 98%). In conclusion, high-altitude residents living at 4,243 m have almost total loss of cerebral autoregulation, which improved during oxygen administration. Those people living at 3,440 m and lower have still functioning cerebral autoregulation. This study showed that the altitude region between 3,440 and 4,243 m, marked by Sa(O(2)) in the high-altitude dwellers of 93% and 88%, is a transitional zone, above which cerebral autoregulation becomes critically impaired.

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