Brain blood flow in Andean and Himalayan high-altitude populations: evidence of different traits for the same environmental constraint.

Humans have populated the Tibetan plateau much longer than the Andean Altiplano. It is thought that the difference in length of occupation of these altitudes has led to different responses to the stress of hypoxia. As such, Andean populations have higher hematocrit levels than Himalayans. In contrast, Himalayans have increased circulation to certain organ systems to meet tissue oxygen demand. In this study, we hypothesize that cerebral blood flow (CBF) is higher in Himalayans than in Andeans. Using a MEDLINE and EMBASE search, we included 10 studies that investigated CBF in Andeans and Himalayans between 3,658 and 4,330 m altitude. The CBF values were corrected for differences in hematocrit and arterial oxygen saturation. The data of these studies show a mean hematocrit of 50% in Himalayans and 54.1% in Andeans. Arterial oxygen saturation was 86.9% in Andeans and 88.4% in Himalayans. The CBF in Himalayans was slightly elevated compared with sea-level subjects, and was 24% higher compared with Andeans. After correction for hematorit and arterial oxygen saturation, CBF was ∼20% higher in Himalayans compared with Andeans. Altered brain metabolism in Andeans, and/or increased nitric oxide availability in Himalayans may have a role to explain this difference in brain blood flow.

Role of the altitude level on cerebral autoregulation in residents at high altitude.

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.

Intraoperative monitoring of brain tissue oxygen and carbon dioxide pressures reveals low oxygenation in peritumoral brain edema.

Brain edema and swelling often complicate surgery for brain tumors. Its pathophysiology is unclear, as is the relationship with brain tissue oxygenation. Our hypothesis was that brain edema around tumor is cytotoxic type caused by impaired local tissue oxygenation due to increased local tissue pressure. Therefore, we monitored brain tissue oxygen pressure (p(ti)O2) and carbon dioxide pressure (p(ti)CO2) in 19 patients undergoing craniotomy for removal of a brain tumor and specifically studied the effect of decompression by dura opening and by tumor removal with respect to the presence of brain swelling. Before craniotomy, multiparameter sensors were inserted into the peritumoral brain tissue guided by MRI-based stereotaxy. In eight patients who had severe brain swelling upon opening of the dura mater, p(ti)O2 immediately rose from 7 +/- 8 mm Hg to 24 +/- 15 mm Hg ( < 0.05), whereas in patients who did not have swelling, p(ti)O2 went from 16 +/- 9 to 18 +/- 10 mm Hg after opening of the dura. The mean p(ti)O2 of all patients at the start of resection of the tumor was 18 +/- 11 mm Hg, and increased to 30 +/- 15 mm Hg after resection was completed ( < 0.05). The effect on p(ti)O2 of raising the FiO2 to 1.0 was limited in this group of patients, as an increase greater than 50% was found in only six of twelve patients. Notably, in six patients, sensor malfunctions or associated hardware problems occurred, prohibiting useful data acquisition. We conclude that brain tissue oxygenation is reduced in the peritumoral area and improves after local tissue pressure relief, especially in patients with brain swelling. Thus, ischemic processes may contribute to brain edema around tumors. Intraoperative p(ti)O2 monitoring may enhance the safety of neuroanesthesia, but the high incidence of failures with this type of sensor remains a matter of concern.

Basilar artery blood flow velocity and the ventilatory response to acute hypoxia in mountaineers.

Hypoxic ventilatory response is higher in successful extreme-altitude climbers than in controls. We hypothesized that these climbers have lower brainstem blood flow secondary to hypoxia which may possibly cause retention of medullary CO(2) and greater ventilatory drive. Using transcranial Doppler, basilar artery blood flow velocity (Vba) was measured at sea level in 7 extreme-altitude climbers and 10 controls in response to 10 min sequential exposures to inspired oxygen fractions (FI(O(2))) of 0.21 (baseline), 0.13, 0.11, 0.10, 0.09, 0.08 and 0.07. Sa(O(2)) was higher in climbers at FI(O(2)) of 0.11 (P<0.05), 0.08 and 0.07 (both P<0.0001). Expired ventilation (VE) increased more (n.s.), and PET(CO(2)) decreased more (n.s.) in the climbers than in controls. Vba did not significantly change in both groups at FI(O(2)) of 0.13-0.09. At FI(O(2)) of 0.08 and 0.07, Vba decreased 21% (P<0.03) and 27% (P<0.01), respectively, in climbers, and increased 29% (P<0.01) and 27% (P<0.01), respectively, in controls. The conflicting effects of hypoxia and hypocapnia on both medullary blood flow and ventilatory drive thus balance out, giving climbers a greater drive and higher Sa(O(2)), despite lower PET(CO(2)) and lower brain stem blood flow.