Intensive Care Medicine Experimental最新文献

{"title":"ESICM LIVES 2026.","authors":"","doi":"10.1186/s40635-026-00962-w","DOIUrl":"10.1186/s40635-026-00962-w","url":null,"abstract":"","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 Suppl 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lymphopenia and elevated NLR identify patients with septic shock who may benefit from corticosteroids: a target trial emulation study.","authors":"Patrick Jason Toppin, Mario Diego Teles Correia, Yale Chang, Lasith Adhikari, Brian McLaverty, Annamalai Natarajan","doi":"10.1186/s40635-026-00972-8","DOIUrl":"10.1186/s40635-026-00972-8","url":null,"abstract":"<p><strong>Background: </strong>Septic shock is the most severe form of sepsis and has high mortality. Despite the widespread use of corticosteroids, evidence of their benefit remains unclear; precision critical care medicine has sought to identify which patients will benefit. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are widely available markers of inflammation and immune function. This study aimed to determine whether these parameters can identify septic shock patients likely to benefit from corticosteroid treatment.</p><p><strong>Methods: </strong>A target trial was emulated using data from the Medical Information Mart for Intensive Care IV database. Adult patients in the ICU for at least 24 h who met the Sepsis-3 definition for septic shock were included. The cohort was divided into those who received corticosteroids and those who did not. Covariates extracted included NLR and PLR. An Augmented Inverse Probability Weighting (AIPW) double-robust estimator was applied to evaluate the effect of corticosteroids on ICU mortality (primary outcome), in-hospital mortality, the need for renal replacement therapy, the duration of vasopressor therapy, and the length of ICU and hospital stay (secondary outcomes). Univariate AUROC was used to compare the predictive performance of the evaluated parameters.</p><p><strong>Results: </strong>5,533 septic shock stays were identified; 1,009 (18.23%) received corticosteroids. The corticosteroid group was much sicker than the control group, with higher Sequential Organ Failure Assessment (SOFA) scores and greater vasopressor requirements. After adjusting for confounding via an AIPW doubly robust estimator, the analysis revealed that lower baseline lymphocyte count (AUROC 0.65), higher NLR (AUROC 0.62), and higher PLR (AUROC 0.63) had modest but consistent ability to identify cases that benefited from corticosteroid therapy, as reflected by reduced ICU mortality. These compared favourably to the use of the maximum SOFA score (AUROC 0.65) and had similar predictive power for all secondary outcomes.</p><p><strong>Conclusion: </strong>Lower lymphocyte count, higher NLR and PLR were associated with an increased likelihood of model-estimated benefit from corticosteroids. Although the predictive power of these markers was modest, their low cost and wide availability could make them appealing in low-resource settings. Further research into these simple parameters to guide the treatment of septic shock is warranted.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Continuous monitoring of endotracheal tube obstructions using naturally occurring pressure and flow oscillations.","authors":"Ben Fabry, Christian Kuster, Roland C E Francis","doi":"10.1186/s40635-026-00982-6","DOIUrl":"10.1186/s40635-026-00982-6","url":null,"abstract":"<p><strong>Background: </strong>The endotracheal tube resistance dominates the total airway resistance in most intubated patients. Mucus deposition and biofilm formation can rapidly increase tube resistance and thereby contribute to serious ventilatory impairments, including dynamic hyperinflation, intrinsic PEEP build-up, added work of breathing, and patient-ventilator asynchrony. During controlled mechanical ventilation, an increased tube resistance can be inferred from the difference between peak and plateau pressure, but this approach fails during pressure-supported spontaneous breathing.</p><p><strong>Methods: </strong>We present a method that estimates the linear and nonlinear components of tube resistance from naturally occurring airway pressure and flow fluctuations at the airway opening, without a tracheal pressure sensor and without imposed forced oscillations. This is achieved by solving the equation of motion using band-pass filtered airway pressure and flow signals. Band-pass filtering isolates the relevant resistive and inertive pressure losses across the tube by removing slow contributions from muscle pressure and lung elastance as well as high-frequency noise.</p><p><strong>Results: </strong>Across different ventilation modes, ventilator settings, tube diameters, filters, and breathing patterns, the method recovers both linear and nonlinear tube resistance parameters with < 10% error and < 2% bias. The method can also track progressive tube obstruction on a breath-by-breath basis.</p><p><strong>Conclusions: </strong>Continuous estimation of the endotracheal tube resistance from naturally occurring, ventilator-induced airway pressure and flow fluctuations enables breath-by-breath detection of tube obstruction and provides the parameters required for automatic tube resistance compensation during spontaneous breathing. This approach may improve patient safety, reduce patient-ventilator asynchrony, and facilitate weaning.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Experimental model of ventilator-induced lung injury induces proteomic signatures of neurodegeneration in the hippocampus.","authors":"Kevin D Winzey, Samuel Guzman, Edward Yang, Debbie Moreira, Xingyu Wang, Xuesong Gu, Simon T Dillon, E Wesley Ely, S Ananth Karumanchi, Towia A Libermann, Shouri Lahiri","doi":"10.1186/s40635-026-00981-7","DOIUrl":"10.1186/s40635-026-00981-7","url":null,"abstract":"<p><strong>Background: </strong>Mechanical ventilation is associated with acute and long-term cognitive dysfunction, yet the molecular pathways linking ventilator-induced lung injury (VILI) to brain injury remain poorly characterized. We previously demonstrated that peripheral IL-6 signaling mediates delirium-like phenotypes in a murine VILI model. Here, we use unbiased aptamer-based proteomics to determine whether this model exhibits proteomic signatures consistent with neurodegenerative processes in the brain and plasma.</p><p><strong>Methods: </strong>C57BL/6 mice were subjected to VILI via high tidal volume mechanical ventilation or served as spontaneously breathing (SB) controls. Brain tissue (hippocampal and cortical regions) and plasma were analyzed using the SomaScan proteomic platform (10,778 and 7,307 proteins, respectively). Differential expression, hierarchical clustering, principal component analysis, and Ingenuity Pathway Analysis (IPA) were performed to identify dysregulated proteins, functional networks, and predicted upstream regulators.</p><p><strong>Results: </strong>SomaScan proteomics identified 253 and 995 significantly altered proteins (p < 0.05) between VILI and SB mice in cortical and hippocampal regions, respectively, and 290 in plasma. Hippocampal pathway analysis revealed enrichment of neurodegeneration, cognitive impairment, and neural differentiation/maturation categories, with dysregulation of proteins including CSNK2A1, SNCA, BDNF, PLD3, and TMEM240. Predicted upstream regulators included CTNNB1, NR3C1, SNCA, and PPARGC1A. Plasma proteomics identified coordinated shifts in metabolic, inflammatory, and vascular injury pathways consistent with an IL-6-associated acute phase response, with predicted activation of HNF4A and PPARG. Only 9 proteins, including PLD3, HAVCR2 (TIM-3), MAG, and STMN4, were dysregulated across all three compartments, with brain-restricted proteins MAG and STMN4 detectable in plasma. The hippocampal region demonstrated the most pronounced alterations, underscoring region-specific vulnerability.</p><p><strong>Conclusions: </strong>VILI induced a dominant hippocampal injury signature enriched for neurodegeneration, cognitive impairment, and disrupted neuronal maturation. Parallel plasma shifts were consistent with inflammatory-metabolic stress and identified a concurrent peripheral response potentially relevant to the lung-brain axis, while detection of brain-restricted proteins in plasma raises the possibility of blood-brain barrier compromise or CNS protein release. Together, these findings support a model in which peripheral lung injury activates coordinated peripheral and hippocampal neuroinflammatory pathways implicated in neurodegenerative biology.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Personalized fluid resuscitation may reduce mortality in septic shock as compared with fixed-volume approach - a systematic review and meta-analysis of randomized controlled trials.","authors":"Gábor Nagy, Júlia Hollósi, Caner Turan, Dávid Laczkó, Zoltán Sipos, Péter Hegyi, László Zubek, Zsolt Molnár","doi":"10.1186/s40635-026-00967-5","DOIUrl":"10.1186/s40635-026-00967-5","url":null,"abstract":"<p><strong>Introduction: </strong>Immediate fluid resuscitation plays a pivotal role in sepsis management. It remains unclear whether a fixed-volume or personalized strategy is more beneficial. Our aim was to compare effectiveness and safety of personalized vs. fixed-volume resuscitation in septic patients in a systematic review and meta-analysis.</p><p><strong>Methods: </strong>We conducted a systematic literature search on PubMed, EMBASE and CENTRAL on October 30, 2024. The pre-study protocol was registered with PROSPERO (ID: CRD42024601970). Randomized controlled trials investigated septic patients who received fluid therapy in a personalized way during their initial resuscitation and reported the outcomes of our interest. The meta-analysis was performed using META packages in R with a random-effects model. Risk of bias was assessed using RoB2.</p><p><strong>Results: </strong>The selection yielded 10 eligible randomized controlled trials (RCTs) with 1,011 patients. Data from 8 RCTs (n = 901) revealed significantly reduced odds of 30-day mortality, (OR: 0.62; 95% CI: 0.42-0.93); however, there was no significant difference in the requirement for renal replacement therapy (OR: 0.77; 95% CI: 0.23-2.55), duration of mechanical ventilation (MD: 0.27; 95% CI: -3.09-3.63), vasopressor therapy (MD: -3.70; 95% CI: -32.88-25.48) and length of hospital (MD: -0.87; 95% CI: -4.97-3.25) or intensive care unit stay (MD: 0.44; 95% CI: -1.90-2.77).</p><p><strong>Conclusion: </strong>Personalized fluid resuscitation, compared with fixed-volume resuscitation, indicated reduced 30-day mortality in septic patients. However, the observed mortality benefit should be interpreted cautiously given the relatively small overall sample size, predominance of small single-center studies, and moderate-to-low certainty of evidence.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and evaluation of machine learning-based prediction-modelling for initial vancomycin serum concentrations in septic ICU patients using clinical health record data.","authors":"Robin Grugel, Britta Westhus, Hartmuth Nowak, Michael Adamzik, Tim Rahmel, Martin Eisenacher","doi":"10.1186/s40635-026-00973-7","DOIUrl":"10.1186/s40635-026-00973-7","url":null,"abstract":"<p><strong>Background: </strong>Sepsis remains a life-threatening condition with highly heterogeneous and dynamic pathophysiology, limiting the effectiveness of uniform therapeutic strategies. Beyond timely source control, antimicrobial therapy represents the only causal treatment option. Vancomycin is widely used for treatment of Gram-positive infections; however, optimal dosing in septic patients is challenging due to pronounced pharmacokinetic variability and substantial interindividual heterogeneity. Underdosing may promote antimicrobial resistance, whereas overdosing increases the risk of toxicity. This study aimed to develop and validate a machine learning-based prediction model to support individualized vancomycin dosing using routinely available clinical data.</p><p><strong>Methods: </strong>This single-center retrospective study included adult sepsis patients admitted to the intensive care unit, using routinely collected data from the hospital's electronic medical records. Patients were eligible if they received a vancomycin loading dose followed by continuous infusion and had at least one measured serum concentration. Three machine learning models-elastic net regression, random forest, and XGBoost-were developed to predict the initial vancomycin serum concentration. To minimize bias and enhance generalizability, model training, hyperparameter tuning, and performance evaluation were conducted using a stratified nested cross-validation approach. Model performance was compared with seven commonly used population pharmacokinetic models.</p><p><strong>Results: </strong>The developed best performing elastic net model achieved a notable improvement with an average RMSE of 6.19, compared to 7.83 for the best pharmacokinetic model highlighting the potential of early and individualized dosing supported by a machine learning model. Final model analysis revealed that noradrenaline administration, together with classical pharmacokinetic parameters including body weight, serum creatinine, and the presence of chronic kidney disease, significantly influenced predictive performance.</p><p><strong>Conclusions: </strong>This machine learning-based approach for predicting initial vancomycin serum concentrations outperforms conventional PK models and enables more precise, individualized dosing prior to the availability of therapeutic drug monitoring results. By integrating key clinical variables, the model facilitates data-driven decision-making in sepsis care and underscores the potential of machine learning to advance personalized antimicrobial therapy.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13601424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Automated hemodynamic resuscitation system for computer-controlled norepinephrine, vasopressin, and fluid therapy in endotoxin-induced shock: a feasibility and physiological proof-of-concept study.","authors":"Kazumasu Sasaki, Kazunori Uemura, Hiroki Matsushita, Yuta Nakamura, Kenta Ohba, Yasuyuki Kataoka, Takuya Nishikawa, Kei Sato, Hidetaka Morita, Masahiro Otake, Nana Hiraki, Masafumi Fukumitsu, Toru Kawada, Kenji Sunagawa, Joe Alexander, Keita Saku","doi":"10.1186/s40635-026-00977-3","DOIUrl":"10.1186/s40635-026-00977-3","url":null,"abstract":"<p><strong>Background: </strong>To support hemodynamic management in vasoplegic shock, we previously developed a closed-loop automated infusion system of norepinephrine (NE) and fluid to automatically restore arterial pressure (AP) and cardiac output (CO). To enhance the practical feasibility and efficacy of the system, we integrated a minimally invasive CO monitor and a closed-loop control of vasopressin (AVP) infusion to the system and validated the integrated system in dogs with endotoxin-induced shock.</p><p><strong>Methods: </strong>Based on the circulatory equilibrium framework, the system directly controls systemic vascular resistance and stressed blood volume by titrating NE and Ringer's acetate solution (RiA), respectively, thereby restoring AP and CO. AVP is automatically initiated once infusion rate of NE is increased higher than 1 μg·kg⁻¹·min⁻¹. The minimally invasive CO monitor estimates CO (CO_es) by a machine-learning analysis of the peripheral AP contour. In eight anesthetized dogs, the system was implemented, and reference CO (CO_ref) was measured using an aortic flow probe to calibrate CO_es and track reference hemodynamics. Endotoxin shock was induced via intravenous lipopolysaccharide infusions. After the target AP and CO_es were set to 70 mmHg and 132 (132-133) mL·min^-1·kg^-1, respectively, the system was activated.</p><p><strong>Results: </strong>The lipopolysaccharide infusion significantly reduced AP from 82 (80-85) to 52 (50-56) mmHg and CO_ref from 132 (125-146) to 90 (80-103) mL·min^-1·kg^-1, and increased the blood lactate level (LAC) from 21 (21-23) to 36 (32-38) mg·dL^-1. Once the system was activated, infusions of NE and RiA were automatically initiated. Infusion of AVP initiated during the system control was associated with significant reduction in NE dose while maintaining AP. Within 5 min after system activation, AP and CO_es were recovered to >65 mmHg and >122 (122-123) ml·min^-1·kg^-1, respectively. The median absolute performance errors for AP and CO_es were <5%. At 60 min after system activation, AP and CO_ref significantly increased to 72 (68-75) mmHg and 130 (127-137) ml·min^-1·kg^-1 and LAC significantly decreased to 26 (25-28) mg·dL^-1 relative to the values observed at endotoxin shock. CO_es tracked directional changes in CO_ref reasonably well.</p><p><strong>Conclusions: </strong>This proof-of-concept study validates the feasibility and physiological performance of the system for the hemodynamic management of vasoplegic shock.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13590466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertonic sodium lactate improves microcirculation, modulates inflammation, and preserves vascular reactivity in a rat model of sepsis: in vivo and ex vivo evidence.","authors":"Eva Correia, Thomas Maudhuizon, Antoine Hérault, Soumeya Bekri, Eric Fontaine, Jérémy Bellien, Paul Mulder, Fabienne Tamion, Emmanuel Besnier","doi":"10.1186/s40635-026-00975-5","DOIUrl":"10.1186/s40635-026-00975-5","url":null,"abstract":"<p><strong>Background: </strong>Hypertonic sodium lactate (HSL) has demonstrated beneficial effects in experimental sepsis, improving hemodynamics, modulating inflammation, and supporting cellular metabolism. Nevertheless, prior studies have not specifically addressed microcirculation, despite its critical impairment during sepsis and the absence of targeted therapies. We evaluated the therapeutic effects of HSL in a in vivo resuscitated rat model (Male wistars) of cecal ligation and puncture (CLP), with a particular focus on microcirculatory function, followed by ex vivo investigation of sodium lactate on vascular reactivity.</p><p><strong>Results: </strong>10 h after CLP rats were infused with 0.9% NaCl or 11.2% HSL for 18 h before exploration. No difference was observed on arterial pressure, echocardiography and pressure-volume loops. HSL improved mesenteric perfusion (1126 [923-1300] vs. 816.5 [692-919] Perfusion Unit, p = 0.012) and TNF-α plasma levels (26.2 [22.8-37.1] vs. 42.6 [32.6-47.3] pg/mL, p = 0.001). Ex vivo, mesenteric artery reactivity experiments from healthy rats was tested with or without LPS-stimulation and glucose deprivation. Lactate dose-dependently restored LPS-impaired vasoconstriction, showing an independent effect on small arteries. In glucose deprivation conditions, HSL was able to restore vascular reactivity in normal or LPS-stimulated arteries.</p><p><strong>Conclusions: </strong>HSL specifically improved microcirculation and reduced systemic inflammation in septic rats. Moreover, lactate may act as an alternative to glucose in deprivation conditions. These benefits support its translational potential as a resuscitation fluid in sepsis.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13590461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remote intestinal changes following blast-induced thoracic trauma with transient hemorrhagic shock and hind-limb ischemia.","authors":"Sophie Meisen, Lena Doerfer, Marco Mannes, Annette Palmer, Frank Hildebrand, Alexander Kleger, Rebecca Halbgebauer, Markus Huber-Lang","doi":"10.1186/s40635-026-00970-w","DOIUrl":"10.1186/s40635-026-00970-w","url":null,"abstract":"<p><strong>Background: </strong>The intestine is both a driver and a target of posttraumatic organ dysfunction. However, it remains unclear whether, and to what extent an extra-abdominal trauma, such as thoracic trauma with transient hemorrhagic shock and hind-limb ischemia (THS), provokes remote intestinal alterations.</p><p><strong>Methods: </strong>A post hoc analysis was performed using jejunal tissue from a standardized murine THS model. Histological, immunohistochemical, and molecular analyses evaluated epithelial integrity, barrier components, and immune responses 24 h after the insult.</p><p><strong>Results: </strong>Histological assessment of the intestine revealed no overt morphological damage. Nonetheless, jejunal expression of Tnk1 and Ripk3 was significantly increased, indicating epithelial stress and activation of necroptotic signaling. Tight junction marker Tjp1 was upregulated, while Muc2 was reduced. Intestinal expression levels of Il6 and Ifng declined, paralleled by a decrease in CD3⁺ T cells, whereas Lcn2 levels increased.</p><p><strong>Conclusions: </strong>Thoracic trauma combined with transient hemorrhagic shock including hind-limb ischemia induces remote intestinal alterations, characterized by epithelial stress, compensatory barrier reinforcement, and reduced mucosal immunity. These findings highlight the gut's sensitivity to extra-abdominal trauma and its potential contribution to systemic injury propagation.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic hypercapnia after cardiac arrest: still promising or time to move on?","authors":"Wiput Laosuksri, Borwon Wittayachamnankul, Siriporn C Chattipakorn, Nipon Chattipakorn","doi":"10.1186/s40635-026-00974-6","DOIUrl":"10.1186/s40635-026-00974-6","url":null,"abstract":"<p><p>Post-cardiac arrest care remains challenging, with persistently poor neurological and survival outcomes. Accordingly, novel adjunctive interventions are needed. While maintaining normocapnia is the current standard, hypercapnia has been proposed as a potential intervention. However, its role and potential benefits remain unclear. This comprehensive review summarizes current evidence on the use of hypercapnia in post-cardiac arrest care, focusing on neurological, cardiovascular, and survival outcomes, underlying mechanisms, and directions for future clinical investigations. Observational studies have sparked interest in the potential benefits of hypercapnia during the post-cardiac arrest period, including in specific populations. Methodological variations and conflicting findings from earlier studies have prompted the conduct of controlled trials and animal experiments to clarify its effects. Mild hypercapnia appears to be a practical and clinically safe approach, improving cerebral oxygenation without major adverse events. However, no improvement in long-term neurological recovery or survival has been demonstrated. Moreover, the effects on the cardiovascular and other organ systems, as well as mechanisms at the cellular level, remain inconclusive. Although mild hypercapnia may be considered part of a comprehensive post-cardiac arrest care strategy, further studies are needed to define its optimal application, potential synergy with other interventions, the populations most likely to benefit, and its underlying mechanisms.</p>","PeriodicalId":13750,"journal":{"name":"Intensive Care Medicine Experimental","volume":"14 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}