ArticleBrain circulation
The impact of high-altitude and cold environment on brain and heart damage in rats with hemorrhagic shock.
Article in Brain circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed.
- Inflammation in Idiopathic Intracranial Hypertension: An Immunometabolic Mechanistic Framework and Clinical Implications.CNS neuroscience & therapeutics · 2026Review
- Short-term high-altitude exposure protects working memory by balancing intestinal microbiota.BMC microbiology · 2026Article
- Host stress proteins shape hemorrhagic shock via gut microbiota: evidence from Mendelian randomization and animal models.Journal of translational medicine · 2025Article
- Understanding the mechanistic and therapeutic perspectives on cytokines and chemokines in acute high-altitude illness syndromes.Journal of pharmaceutical analysis · 2025Review
- Cold exposure and the cardiovascular system: from physiological adaptation to pathological risk.Frontiers in physiology · 2025Review
- TBC1D15 Inhibits Autophagy of Microglia through Maintaining the Damaged Swelling Lysosome in Alzheimer's Disease.Aging and disease · 2024Article
- Immune alterations in vestibular neuritis: a retrospective database pilot study on T and B lymphocyte profiles and cytokine levels.Frontiers in neurologyArticle
- Protective effects of hypoxic conditioning treatment on brain and cardiac tissues following thoracic aorta occlusion.Brain circulationArticle
- Concurrent VVOR and VORS profiling reveals a threshold-dependent VOR suppression deficit in vestibular migraine.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHemorrhagic shock (HS) causes severe organ damage, worsened by high-altitude conditions with lower oxygen and temperatures. Existing research lacks specific insights on brain and heart damage under these conditions. This study hypothesizes that high-altitude and cold (HAC) environments exacerbate HS-induced damage in the brain and heart, aiming to improve treatment strategies. MATERIALS AND
methodsTwenty-four male Sprague-Dawley (SD) rats (200-250 g of weight) were randomly assigned into sham, HS + normal, HS + HAC (4,000 m), and HS + HAC (6,000 m). The HS model was established in SD rats (35% loss of total blood volume), and histopathological injuries of the brain and heart were detected using hematoxylin and eosin staining, Sirius red staining, and immunohistochemistry. Apoptosis of the brain and heart tissues was detected by terminal transferase-mediated dUTP nick end labeling (TUNEL) immunofluorescence staining. To determine the levels of tumor necrosis factor-α (TNF-α), interferon-gamma (IFN-γ), monocyte chemoattractant protein-1 (Mcp-1), BCL2-associated X (BAX), and myeloid cell leukemia-1 (Mcl-1) protein, western blotting assay was used.
resultsThe HAC environment induced pathological damage to the brain and heart and aggravated the degree of cardiac fibrosis in HS rats. However, it did not cause apoptosis of the brain and heart. In addition, it upregulated TNF-α, IFN-γ, Mcp-1, and BAX protein levels, but downregulated Mcl-1 protein levels (
conclusionsThe HAC environment aggravated the degree of brain and heart damage in HS rats, which may be related to neuron nucleus pyknosis, myocardial fibrosis, and inflammatory and apoptosis activation.
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.