Background: Hemorrhagic shock is known to disrupt the gut barrier leading to end-organ dysfunction. The vagus nerve can inhibit detrimental immune responses that contribute to organ damage in hemorrhagic shock. Therefore, we explored whether stimulation of the vagus nerve can protect the gut and recover lung permeability in trauma-hemorrhagic shock (THS).
Methods: Male Sprague-Dawley rats were subjected to left cervical vagus nerve stimulation at 5 V for 10 minutes. The right internal jugular and femoral artery were cannulated for blood withdrawal and blood pressure monitoring, respectively. Animals were then subjected to hemorrhagic shock to a mean arterial pressure between 30 mm Hg and 35 mm Hg for 90 minutes then reperfused with their own whole blood. After observation for 3 hours, gut permeability was assessed with fluorescein dextran 4 in vivo injections in a ligated portion of distal ileum followed by Evans blue dye injection to assess lung permeability. Pulmonary myeloperoxidase levels were measured and compared.
Results: Vagal nerve stimulation abrogated THS-induced lung injury (mean [SD], 8.46 [0.36] vs. 4.87 [0.78]; p < 0.05) and neutrophil sequestration (19.39 [1.01] vs. 12.83 [1.16]; p < 0.05). Likewise, THS gut permeability was reduced to sham levels.
Conclusion: Neuromodulation decreases injury in the THS model as evidenced by decreased gut permeability as well as decreased lung permeability and pulmonary neutrophil sequestration in a rat model.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3683843 | PMC |
| http://dx.doi.org/10.1097/TA.0b013e31825debd3 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Disorders in pulmonary vascular integrity are a prominent feature in many lung diseases. Paracrine signaling is highly enriched in the lung and plays a crucial role in regulating vascular homeostasis. However, the specific local cell-cell crosstalk signals that maintain pulmonary microvascular stability in adult animals and humans remain largely unexplored.
View Article and Find Full Text PDFHyaluronan Directs Alveolar Type II Cell Response to Acute Ozone Exposure in Mice.
Am J Respir Cell Mol Biol
January 2025
Duke Medicine, Medicine, Durham, North Carolina, United States.
Becoming more frequent due to climate change, ozone (O) exposures can cause lung injury. Alveolar type 2 (AT2) cells and hyaluronan (HA), a matrix component, are critical to repairing lung injury and restoring homeostasis. Here, we define the impact of HA on AT2 cells following acute O exposure.
View Article and Find Full Text PDFβ-Caryophyllene attenuates oxidative stress and inflammatory response in LPS induced acute lung injury by targeting ACE2/MasR and Nrf2/HO-1/NF-κB axis.
Biochem Biophys Res Commun
January 2025
Division of Pharmaceutical Technology, Defence Research Laboratory, DRDO, Tezpur, Assam, 784001, India. Electronic address:
Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), is a clinical syndrome that can cause pulmonary edema, inflammation, oxidative stress, and immunological dysregulations. β-Caryophyllene (BCP), a natural bicyclic sesquiterpene, possesses a variety of pharmacological properties and has the potential to be a therapeutic agent. This study aimed to comprehend the effect of BCP on Nrf2/HO-1/NF-κB and ACE2/MasR axis in a rat model of ALI by lipopolysaccharide (LPS) and the underlying mechanisms during this process.
View Article and Find Full Text PDFElectroacupuncture promotes resolution of inflammation by modulating SPMs via vagus nerve activation in LPS-induced ALI.
Int Immunopharmacol
January 2025
Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, China; Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin, China. Electronic address:
During the process of acute lung injury (ALI) associated with sepsis, the α7nAChR in the cholinergic anti-inflammatory pathway (CAP) plays a crucial role. However, the roles of electroacupuncture (EA) and specialized pro-resolving mediators (SPMs) in this context remain unclear. In this study, we demonstrated that EA activates CAP via α7nAChR, reducing lung permeability and inflammatory cytokine release.
View Article and Find Full Text PDFReceptor-Interacting Protein Kinase 3-Mediated Modulation of Endothelial Cell Necroptosis and Mitochondrial Dysfunction through AMPK/Drp1 Signaling Pathway: Insights into the Pathophysiological Mechanisms of Lipopolysaccharide-Induced Acute Lung Injury.
Int J Med Sci
January 2025
Health Management Institute, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing 100853, China.
Article Synopsis
- Ripk3 is key in acute lung injury (ALI) by driving endothelial cell damage and inflammation, although the exact mechanisms are not fully understood.
- Studies using Ripk3-deficient mice revealed that removing Ripk3 improved lung tissue health, decreased inflammation, oxidative stress, and endothelial dysfunction after exposure to lipopolysaccharide (LPS).
- Ripk3 was found to inhibit the AMPK pathway and promote necroptosis in endothelial cells by affecting mitochondrial function, suggesting it could be a target for new treatments for ALI.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!