Trial reportJournal of applied physiology (Bethesda, Md. : 1985)2011
Acute mountain sickness, inflammation, and permeability: new insights from a blood biomarker study.
Trial report in Journal of applied physiology (Bethesda, Md. : 1985), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 102 citations in OpenAlex.
- Pooled it
- Interventions for preventing high altitude illness: Part 1. Commonly-used classes of drugs.The Cochrane database of systematic reviews · 2017Pooled it
- Efficacy of ibuprofen on prevention of high altitude headache: A systematic review and meta-analysis.PloS one · 2017Pooled it
- Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema.Mediators of inflammation · 2016Trial
- MRI evidence: acute mountain sickness is not associated with cerebral edema formation during simulated high altitude.PloS one · 2012Trial
- Oxygen physiology and mechanisms of oxygen toxicity: a narrative review.Medical gas research · 2026Review
- G Protein-Coupled Receptor in High-Altitude Diseases: Mechanistic Insights and Therapeutic Opportunities.MedComm · 2026Review
- Biomarkers and potential subtypes of acute mountain sickness: A state-of-the-science review.Redox biology · 2026Review
- Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026Review
- Mitochondrial retrograde signaling initiates HIF-1α/BNIP3/NIX-mediated mitophagy in Tibetan high-altitude adaptation.Cell death discovery · 2026Article
- Xinnaoxin tablets ameliorate high-altitude polycythemia-associated cardiac injury by regulating the NF-κB, MAPK, and PI3K/AKT signaling pathways.Frontiers in pharmacology · 2026Article
- Effects of mitochondrial gene mutation 8923 (A→G) on inflammatory indicators and blood pressure after acute high-altitude exposure.Frontiers in physiology · 2026Article
- Low hypoxia tolerance as a determinant of the proinflammatory phenotype: a trained immunity perspective.Frontiers in immunology · 2026Review
- Integrated proteomic and metabolomic analyses define the molecular architecture of acute mountain sickness.Frontiers in genetics · 2026Article
- Acute high-altitude hypoxia induced NLRP3 inflammasome activation in pulmonary artery smooth muscle cells by BMAL1 targeting mitochondrial VDAC1-mediated MtDNA leakage.Apoptosis : an international journal on programmed cell death · 2025Article
- Understanding the mechanistic and therapeutic perspectives on cytokines and chemokines in acute high-altitude illness syndromes.Journal of pharmaceutical analysis · 2025Review
- Machine learning integration identifying an eight-gene diagnostic signature for acute mountain sickness.Frontiers in medicine · 2025Article
- Astaxanthin Supplementation Effects in Right Ventricle of Rats Exposed to Chronic Intermittent Hypobaric Hypoxia.Antioxidants (Basel, Switzerland) · 2024Article
- Altitude illnesses.Nature reviews. Disease primers · 2024Review
- Inflammation severity, rather than respiratory failure, is strongly associated with mortality of ARDS patients in high-altitude ICUs.Frontiers in physiology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The pathophysiology of acute mountain sickness (AMS) is unknown. One hypothesis is that hypoxia induces biochemical changes that disrupt the blood-brain barrier (BBB) and, subsequently, lead to the development of cerebral edema and the defining symptoms of AMS. This study explores the relationship between AMS and biomarkers thought to protect against or contribute to BBB disruption. Twenty healthy volunteers participated in a series of hypobaric hypoxia trials distinguished by pretreatment with placebo, acetazolamide (250 mg), or dexamethasone (4 mg), administered using a randomized, double-blind, placebo-controlled, crossover design. Each trial included peripheral blood sampling and AMS assessment before (-15 and 0 h) and during (0.5, 4, and 9 h) a 10-h hypoxic exposure (barometric pressure = 425 mmHg). Anti-inflammatory and/or anti-permeability [interleukin (IL)-1 receptor agonist (IL-1RA), heat shock protein (HSP)-70, and adrenomedullin], proinflammatory (IL-6, IL-8, IL-2, IL-1β, and substance P), angiogenic, or chemotactic biomarkers (macrophage inflammatory protein-1β, VEGF, TNF-α, monocyte chemotactic protein-1, and matrix metalloproteinase-9) were assessed. AMS-resistant subjects had higher IL-1RA (4 and 9 h and overall), HSP-70 (0 h and overall), and adrenomedullin (overall) compared with AMS-susceptible subjects. Acetazolamide raised IL-1RA and HSP-70 compared with placebo in AMS-susceptible subjects. Dexamethasone also increased HSP-70 and adrenomedullin in AMS-susceptible subjects. Macrophage inflammatory protein-1β was higher in AMS-susceptible than AMS-resistant subjects after 4 h of hypoxia; dexamethasone minimized this difference. Other biomarkers were unrelated to AMS. Resistance to AMS was accompanied by a marked anti-inflammatory and/or anti-permeability response that may have prevented downstream pathophysiological events leading to AMS. Conversely, AMS susceptibility does not appear to be related to an exaggerated inflammatory response.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.