ArticleAnnals of surgery2014
Intraluminal nonbacterial intestinal components control gut and lung injury after trauma hemorrhagic shock.
Article in Annals of surgery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
- Remote Pancreatic Response to Severe Polytrauma Correlates With Clinical Outcome.United European gastroenterology journal · 2026Article
- RIPK3 Protects Against Endothelial Activation and Vascular Permeability in a Mouse Model of Ischemia-Reperfusion Injury.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Oxygen-Mediated Molecular Mechanisms Involved in Intestinal Ischemia and Reperfusion Injury.International journal of molecular sciences · 2025Review
- Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Inhibition of miR-142-3p promotes intestinal epithelial proliferation and barrier function after ischemia/reperfusion injury by targeting FoxM1.Molecular and cellular biochemistry · 2025Article
- Intestinal oxygen utilisation and cellular adaptation during intestinal ischaemia-reperfusion injury.Clinical and translational medicine · 2025Review
- Navigating Hemorrhagic Shock: Biomarkers, Therapies, and Challenges in Clinical Care.Biomedicines · 2024Review
- Protopine-Type Alkaloids Alleviate Lipopolysaccharide-Induced Intestinal Inflammation and Modulate the Gut Microbiota in Mice.Animals : an open access journal from MDPI · 2024Article
- Role of the antioxidant pathway in the healing of peptic ulcers induced by ischemia-reperfusion in male and female rats treated with Eugenia punicifolia.Inflammopharmacology · 2022Article
- Mast Cells Drive Systemic Inflammation and Compromised Bone Repair After Trauma.Frontiers in immunology · 2022Article
- The Reaction Pathway of miR-30c-5p Activates Lipopolysaccharide Promoting the Course of Traumatic and Hemorrhagic Shock Acute Lung Injury.BioMed research international · 2022Article
- NLRX1/FUNDC1/NIPSNAP1-2 axis regulates mitophagy and alleviates intestinal ischaemia/reperfusion injury.Cell proliferation · 2021Article
- Pathophysiology and protective approaches of gut injury in critical illness.Yeungnam University journal of medicine · 2021Article
- Aggravated intestinal ischemia‑reperfusion injury is associated with activated mitochondrial autophagy in a mouse model of diabetes.Molecular medicine reports · 2020Article
- Pancreatic secretory trypsin inhibitor reduces multi-organ injury caused by gut ischemia/reperfusion in mice.PloS one · 2020Article
- Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Metabolomics analysis of gut barrier dysfunction in a trauma-hemorrhagic shock rat model.Bioscience reports · 2019Article
- Gut integrity in critical illness.Journal of intensive care · 2019Review
- Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury viaOxidative medicine and cellular longevity · 2019Article
- Inhibition of ubiquitin-activating enzyme protects against organ injury after intestinal ischemia-reperfusion.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo test whether the mucus layer, luminal digestive enzymes, and intestinal mast cells are critical components in the pathogenesis of trauma shock-induced gut and lung injury.
backgroundGut origin sepsis studies have highlighted the importance of the systemic component (ischemia-reperfusion) of gut injury, whereas the intraluminal component is less well studied.
methodsIn rats subjected to trauma hemorrhagic shock (T/HS) or sham shock, the role of pancreatic enzymes in gut injury was tested by diversion of pancreatic enzymes via pancreatic duct exteriorization whereas the role of the mucus layer was tested via the enteral administration of a mucus surrogate. In addition, the role of mast cells was assessed by measuring mast cell activation and the ability of pharmacologic inhibition of mast cells to abrogate gut and lung injury. Gut and mucus injury was characterized functionally, morphologically, and chemically.
resultsPancreatic duct exteriorization abrogated T/HS-induced gut barrier loss and limited chemical mucus changes. The mucus surrogate prevented T/HS-induced gut and lung injury. Finally, pancreatic enzyme-induced gut and lung injury seems to involve mast cell activation because T/HS activates mast cells and pharmacologic inhibition of intestinal mast cells prevented T/HS-induced gut and lung injury.
conclusionsThese results indicate that gut and gut-induced lung injury after T/HS involves a complex process consisting of intraluminal digestive enzymes, the unstirred mucus layer, and a systemic ischemic-reperfusion injury. This suggests the possibility of intraluminal therapeutic strategies.
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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.