Abstract
Altitude-Limited Fetal Growth Linked to Uterine Arteriolar Resistance
Browne et al (2011) report the first quantitative measurements demonstrating that uterine arteriolar resistance limited blood flow in 20 high altitude pregnancies with early onset preeclampsia (PE). They compared uterine arterial, common iliac and external iliac arterial blood flow with data from 3 other groups of Andeans also residing at 3600-4100 m, 23 non-pregnant, 155 normotensive pregnant, and 12 with gestational hypertension (GH). Blood flow was lower and end-arteriolar vascular resistance was higher in both PE and GH. Women with early onset PE delivered early, with 43% of babies stillborn. Those with GH and late onset PE delivered at term, but half were small. Birth weight, disease severity and adverse fetal outcomes were strongly associated with reduced uterine arterial blood flow.
Risk Factors of High Altitude Headache
Burtscher et al (2011) interviewed 506 alpine hikers after their first night at huts between 2200 and 3817 m altitude. High-altitude headache occurred in 31%. A migraine history, lower than expected arterial oxygen saturation, high ratings of perceived exertion and fluid intake below 2 l were identified as independent risk factors.
VEGF-A Gene Related to Acute Mountain Sickness
Ding et al (2011) evaluated single-nucleotide polymorphisms (SNPs) of 4 hypoxia-related genes (HIF-1, VEGFA, HSP-70 and eNOS) in 128 Chinese males after 24 hr at 4600 m altitude, half of whom had acute mountain sickness (AMS) by Lake Louise scores. Twenty-eight of the 48 SNPs investigated were successfully genotyped, and SNP allele frequencies were obtained. The rs3025039 SNP and the haplotypes (rs1413711, rs833070 and rs3025000) in the VEGFA gene were significantly associated with AMS (p = 0.0435 and 0.024, respectively).
Sleeping in Hypoxia at Sea Level Improves Later Sleep Saturation and Morning Acute Mountain Sickness (AMS) at Altitude
The possibility of pre-acclimatizing at sea level before going to altitude was studied by Fulco et al (2011). 14 subjects slept for 7.5 h each night for 7 consecutive nights in rooms at gradually reduced O2 (16.2% to 14.3%), simulating 2200 m to 3100 m, before moving for 5 days to 4300 m altitude. PetCO2 decreased from 39 to 35 torr before ascent. Mean sleep SaO2 after ascent was 80% compared with 76% in 9 controls (P<0.05). AMS scores upon awakening were lower than in controls (P<0.02). The higher sleep SaO2 had no impact on AMS or exercise performance for the remainder of each day.
Children at High Altitude Need Less Post-Operative Opioid Pain Relief
Hypoxia has been shown to enhance the analgesic effect of opioids in both animals and children with obstructive sleep apnea. As part of a surgical and anesthesia team repairing cleft lip or palate defects at both high and low altitudes in Peru, Rabbitts et al (2010) reviewed retrospectively the post operative opioid requirements of 102 children in Cuzco, 3399 m altitude and 169 in Lima at sea level. Anesthetic methods were standardized and only intravenous fentanyl was used for post-operative pain relief. In Cuzco, the needed opioid dose was 40% lower (P<0.001). In Cuzco, baseline SpO2 was 92 ± 4% vs 98 ± 3% in Lima. It remains unknown whether hypoxia reduces post-surgical pain or intensifies narcotic potency.
Exercise Desaturation at Sea Level Correlates With Impaired Performance at Altitude
Chapman et al (2011) show that the degree of arterial desaturation found in treadmill testing at sea level in 27 elite runners predicted the impairment of their running performance at 2100 m altitude. Seven of the group in whom SaO2 fell below 91% while running at their 3000 m speed at sea level were compared with 7 who maintained SaO2 > 93%. The increase in 3000 m time at 2100 m altitude was significantly more in the low saturation group, 54.0 ± 13.7s vs 38.9 ± 9.7s.
Altitude Skeletal Muscle Atrophy Not Due to Decreased Protein Synthesis
Holm et al (2010) report a doubling of myofibrillar protein synthesis rate in 9 healthy subjects after 7-9 days at 4559 m altitude. Sarcoplasmic protein synthesis rate was unaffected by altitude. The authors conclude that whole body amino acid flux is increased at altitude due to an elevated protein turnover rate.
Weight Loss at Extreme Altitude is Primarily Fat-Free Muscle (FFM)
Before and after expeditions to Everest and Gasherbrum, 8 climbers underwent anthropometric measurements, total and regional body composition assessment and handgrip and knee extensor strength measurements by dynamometry. The average FFM loss, 2.4 ± 1.6 kg was mostly from limbs (-2.1 ± 1.4 kg; P < 0.01), and especially upper limbs (-1.6 ± 1.1 kg; P < 0.01). The isotonic knee extensor strength declined in 6 of the 8 study participants, with a mean drop of −4.4 ± 6.1 kg (ns) (Sergi et al., 2010).
Pulmonary Hypertension in Amhara Ethiopians at Altitude
In comparison with Andean and European highlanders, Tibetans have little pulmonary hypertension. Hoit et al (2011) report somewhat elevated mean pulmonary arterial systolic pressure (by echo) of 27.9 ± 8.4 torr in 76 healthy adult Amhara lifelong residents at 3700 m, compared with 21.9 ± 4.0 in 54 Amhara lifelong residents at 1200 m, and 16.5 ± 3.6 torr in a reference sample of 46 U.S. low-altitude residents.
Genetic Differences in Chinese Railway Workers with High Altitude Pulmonary Edema (HAPE)
In 149 HAPE patients among the construction workers and 160 healthy controls, three polymorphisms of eNOS gene, T-786C in promoter, 894G/T in exon 7, and 27bp variable number tandem repeat (VNTR) in intron 4, were genotyped using polymerase chain reaction (PCR) and confirmed with DNA sequencing. The frequencies of the 894T allele and heterozygous G/T of the 894G/T variant were significantly higher in HAPE patients than in controls. However, the frequencies of the T-786C in promoter and the 27bp VNTR in intron 4 were not significantly different between the two groups. Analysis revealed that the frequencies of two haplotypes (H3TTb and H6CGa) were significantly higher in HAPE patients, suggesting a role in susceptibility to HAPE. H1TGb and H2TGa were lower in HAPE patients than in healthy controls (Yu-Jing et al., 2010).
Severe Hypoxic Rat Lung Injury Reduced by Hyperbaric O2 Preconditioning
Hyperbaric O2 preconditioning can reduce subsequent ischemic tissue damage. Li et al (2011) report that the pulmonary damage caused in rats by 24 hr exposure to 6000 m hypobaric hypoxia can be reduced by pretreatment with 100% O2 at 2 ATA for 1 hr per day for 5 days. Injury was scored using histologic alveolar edema, neutrophil infiltration and hemorrhage and as decreased AQP1 and AQP5 lung proteins and mRNA expression.
Cobalt Preconditioning Protects Rat Lung From Severe Hypoxic Injury
Shukla et al (2011) postulated that protection of lung from severe high altitude pulmonary edema by hypoxic preconditioning could be mimicked by cobalt chloride because preconditioning with cobalt has been reported to provide protection in various tissues against ischemic injury. Rats pretreated with saline or cobalt (12.5mg/kg body weight) for 7days were exposed to 9142m hypobaric hypoxia for 5h. Preconditioning with cobalt significantly reduced transvascular leakage of sodium fluorescein dye, lung water content, lavage total protein, albumin, VEGF levels, pro-inflammatory cytokine levels, tissue expression of cell adhesion molecules and NF-κB DNA binding activity after hypoxia. Expression of anti-inflammatory protein HO-1, MT, TGF-β and IL-6 were increased after hypoxic preconditioning. The authors conclude that preconditioning with cobalt may protect against HAPE.