ArticleThe Journal of surgical research2017
Effects of trauma, hemorrhagic shock, and chronic stress on lung vascular endothelial growth factor.
Article in The Journal of surgical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Shock Induced Endotheliopathy and High Trauma Mortality-Fight-or-Flight Response Revisited.International journal of molecular sciences · 2026Review
- Severe traumatic injury is associated with profound changes in DNA methylation.NPJ genomic medicine · 2024Article
- A rat model of multicompartmental traumatic injury and hemorrhagic shock induces bone marrow dysfunction and profound anemia.Animal models and experimental medicine · 2024Article
- Multicompartmental Trauma Induces Persistent Inflammation and Organ Injury.The Journal of surgical research · 2024Article
- Mediators of Prolonged Hematopoietic Progenitor Cell Mobilization After Severe Trauma.The Journal of surgical research · 2021Article
- The effects of selective beta-adrenergic blockade on bone marrow dysfunction following severe trauma and chronic stress.American journal of surgery · 2020Article
- Hypoalbuminemia: Pathogenesis and Clinical Significance.JPEN. Journal of parenteral and enteral nutrition · 2019Review
- Screening and Biosensor-Based Approaches for Lung Cancer Detection.Sensors (Basel, Switzerland) · 2017Review
- Clonidine restores vascular endothelial growth factor expression and improves tissue repair following severe trauma.American journal of surgery · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundVascular endothelial growth factor (VEGF) and its receptors (VEGFR-1 and VEGFR-2) regulate vascular permeability and endothelial cell survival. We hypothesized that hemorrhagic shock (HS) and chronic stress (CS) would increase expression of lung VEGF and its receptors, potentiating pulmonary edema in lung tissue. MATERIALS AND
methodsMale Sprague-Dawley rats aged 8-9 wk were randomized: naïve control, lung contusion (LC), LC followed by HS (LCHS), and LCHS with CS in a restraint cylinder for 2 h/d (LCHS/CS). Animals were sacrificed on days 1 and 7. Expressions of lung VEGF, VEGFR-1, and VEGFR-2 were determined by polymerase chain reaction. Lung Injury Score (LIS) was graded on light microscopy by inflammatory cell counts, interstitial edema, pulmonary edema, and alveolar integrity (range: 0 = normal; 8 = severe injury).
resultsSeven days after LC, lung VEGF and VEGFR-1 were increased, and lung tissue healed (LIS: 0.8 ± 0.8). However, 7 d after LCHS and LCHS/CS, lung VEGF and VEGFR-1 expressions were decreased. VEGFR-2 was also decreased after LCHS/CS. LIS was elevated 7 d after LCHS and LCHS/CS (6.5 ± 1.0 and 8.2 ± 0.8). Increased LIS after LCHS and LCHS/CS was because of higher inflammatory cell counts, increased interstitial edema, and loss of alveolar integrity, whereas pulmonary edema was unchanged.
conclusionsElevation of lung VEGF and VEGFR-1 expressions after LC alone was associated with healing of injured lung tissue. Expressions of VEGF, VEGFR-1, and VEGFR-2 were reduced after LCHS and LCHS/CS, and injured lung tissue did not heal. Persistent lung injury after severe trauma was because of inflammation rather than pulmonary edema.
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