ArticleAlcoholism, clinical and experimental research2014
Acute alcohol intoxication-induced microvascular leakage.
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
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- Role of exchange proteins directly activated by cAMP signaling in vascular remodeling.Pharmacological reviews · 2025Review
- The role of transcytosis in the blood-retina barrier: from pathophysiological functions to drug delivery.Frontiers in pharmacology · 2025Review
- Mechanisms of QiShenYiQi in Inhibiting Blood-Brain Barrier Damage Following Stroke: A Network Pharmacology and Experimental Study.Combinatorial chemistry & high throughput screening · 2025Article
- Imaging and Analysis of the Dynamics of Filamentous Actin Structures in Live Endothelial Cells.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Edema and lymphatic clearance: molecular mechanisms and ongoing challenges.Clinical science (London, England : 1979) · 2023Review
- Changes in Microcirculation in the Brain, Heart, and Liver in Female Rats with Translational Model of Alcoholic Cardiomyopathy.Bulletin of experimental biology and medicine · 2023Article
- Blood Vessels as a Key Mediator for Ethanol Toxicity: Implication for Neuronal Damage.Life (Basel, Switzerland) · 2022Review
- Acute Intoxication With Alcohol Reduces Trauma-Induced Proinflammatory Response and Barrier Breakdown in the LungFrontiers in immunology · 2022Article
- Ethanol-induced lymphatic endothelial cell permeability via MAP-kinase regulation.American journal of physiology. Cell physiology · 2021Article
- Daily Lifestyle and Inflammatory Skin Diseases.International journal of molecular sciences · 2021Review
- The lymphatic system in alcohol-associated liver disease.Clinical and molecular hepatology · 2020Review
- Sphingosine-1-phosphate protects against brain microvascular endothelial junctional protein disorganization and barrier dysfunction caused by alcohol.Microcirculation (New York, N.Y. : 1994) · 2019Article
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- Endothelial Protrusions in Junctional Integrity and Barrier Function.Current topics in membranes · 2018Article
- Differential effects of alcohol and its metabolite acetaldehyde on vascular smooth muscle cell Notch signaling and growth.American journal of physiology. Heart and circulatory physiology · 2018Article
- Assessment of Cardiovascular Function and Microvascular Permeability in a Conscious Rat Model of Alcohol Intoxication Combined with Hemorrhagic Shock and Resuscitation.Methods in molecular biology (Clifton, N.J.) · 2018Review
- Thirst sensation and oral dryness following alcohol intake.The Japanese dental science review · 2017Review
- Sphingosine-1-Phosphate Treatment Can Ameliorate Microvascular Leakage Caused by Combined Alcohol Intoxication and Hemorrhagic Shock.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlcohol intoxication can increase inflammation and worsen injury, yet the mechanisms involved are not clear. We investigated whether acute alcohol intoxication increases microvascular permeability and investigated potential signaling mechanisms in endothelial cells that may be involved.
methodsConscious rats received a 2.5 g/kg alcohol bolus via gastric catheters to produce acute intoxication. Microvascular leakage of intravenously administered fluorescein isothiocyanate (FITC)-conjugated albumin (FITC-albumin) from the mesenteric microcirculation was assessed by intravital microscopy. Endothelial-specific mechanisms were studied using cultured endothelial cell monolayers. Transendothelial electrical resistance (TER) served as an index of barrier function, before and after treatment with alcohol or its metabolite acetaldehyde. Pharmacologic agents were used to test the roles of alcohol metabolism, oxidative stress, p38 mitogen-activated protein kinase (MAPK), myosin light-chain kinase (MLCK), rho kinase (ROCK), and exchange protein activated by cAMP (Epac). VE-cadherin localization was investigated to assess junctional integrity. Rac1 and RhoA activation was assessed by ELISA assays.
resultsAlcohol significantly increased FITC-albumin extravasation from the mesenteric microcirculation. Alcohol also significantly decreased TER and disrupted VE-cadherin organization at junctions. Acetaldehyde significantly decreased TER, but inhibition of alcohol dehydrogenase or application of a superoxide dismutase mimetic failed to prevent alcohol-induced decreases in TER. Inhibition of p38 MAPK, but not MLCK or ROCK, significantly attenuated the alcohol-induced barrier dysfunction. Alcohol rapidly decreased GTP-bound Rac1 but not RhoA during the drop in TER. Activation of Epac increased TER, but did not prevent alcohol from decreasing TER. However, activation of Epac after initiation of alcohol-induced barrier dysfunction quickly resolved TER to baseline levels.
conclusionsOur results suggest that alcohol intoxication increases microvascular permeability to plasma proteins. The data also suggest the endothelial-specific mechanism involves the p38 MAPK, Rac1, and reorganization of VE-cadherin at junctions. Last, activation of Epac can quickly resolve alcohol-induced endothelial barrier dysfunction.
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