SHOCK最新文献

{"title":"THE MITOCHONDRIAL DIVISION INHIBITOR MDIVI-1 PROTECTED ORGAN FUNCTION AND EXTENDED THE TREATMENT WINDOW IN RATS WITH UNCONTROLLED HEMORRHAGIC SHOCK.","authors":"Yi Hu, He Fang, Lei Tan, Han She, Yuanlin Du, Yu Zhu, Yue Wu, Liangming Liu, Tao Li","doi":"10.1097/SHK.0000000000002459","DOIUrl":"10.1097/SHK.0000000000002459","url":null,"abstract":"<p><strong>Abstract: </strong>Aim: This study aimed to elucidate whether the application of the mitochondrial division inhibitor Mdivi-1 can protect organ function and prolong the treatment window for traumatic hemorrhagic shock. Methods: Before definitive hemostasis treatment, Mdivi-1 (0.25 mg/kg, 0.5 mg/kg, and 1 mg/kg) was administered to uncontrolled hemorrhagic shock (UHS) model rats. Lactate Ringer's solution plus hydroxyethyl starch (130/0.4) was used as a control. The effects of Mdivi-1 on blood loss; fluid demand; survival time; vital organ function; myocardial mitochondrial structure; mitochondrial function of the heart, liver, kidney, and intestine; and oxidative stress at 1 h after hypotensive resuscitation (50-60 mm Hg) were investigated. In addition, we investigated the effect of varying doses of Mdivi-1 on the maintenance time of hypotensive resuscitation without definitive hemostasis and the beneficial effect of Mdivi-1 after prolonging the duration of hypotensive resuscitation to 2 h. Results: Compared to conventional resuscitative fluid, Mdivi-1 significantly reduced blood loss and fluid demand, improved important organ functions during hypotensive resuscitation, improved animal survival, and reduced the incidence of early death. Mdivi-1 significantly alleviated oxidative stress injury, reduced mitochondrial damage, and restored myocardial mitochondrial structure and mitochondrial function of the heart, liver, kidney, and intestine. In addition, Mdivi-1 increased the maintenance time of hypotensive resuscitation and improved rat survival after the duration of hypotensive resuscitation was prolonged to 2 h. Conclusion: Mdivi-1 significantly prolonged the treatment window for traumatic hemorrhagic shock to 2 h in UHS model rats. The underlying mechanism may be that Mdivi-1 inhibits excessive mitochondrial fission and oxidative stress and improves the structure and function of mitochondria.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"474-486"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREATMENT WITH THE GLYCOGEN SYNTHASE KINASE-3BETA INHIBITOR, TDZD-8, AFFECTS TRANSIENT CEREBRAL ISCHEMIA/REPERFUSION INJURY IN THE RAT HIPPOCAMPUS [SHOCK. 2008 SEP;30(3):299-307. DOI: 10.1097/SHK.0B013E318164E762].","authors":"","doi":"10.1097/SHK.0000000000002537","DOIUrl":"10.1097/SHK.0000000000002537","url":null,"abstract":"","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":"63 3","pages":"507-508"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beneficial effects of GPI 6150, an inhibitor of poly(ADP-ribose) polymerase in a rat model of splanchnic artery occlusion and reperfusion Shock. 2002 Mar;17(3):222-7. doi: 10.1097/00024382-200,203,000-00011.","authors":"Emanuela Mazzon, Laura Dugo, Angelina De Sarro, Jia-He Li, Achille Caputi, Jie Zhang, Salvatore Cuzzocrea","doi":"10.1097/SHK.0000000000002521","DOIUrl":"10.1097/SHK.0000000000002521","url":null,"abstract":"","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":"63 3","pages":"504"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EFFECT OF THALIDOMIDE ON SIGNAL TRANSDUCTION PATHWAYS AND SECONDARY DAMAGE IN EXPERIMENTAL SPINAL CORD TRAUMA Shock (2008) doi: 10.1097/shk.0b013e318162d290 issn: 1073-2322 pubmed: 18197140.","authors":"","doi":"10.1097/SHK.0000000000002532","DOIUrl":"10.1097/SHK.0000000000002532","url":null,"abstract":"","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":"63 3","pages":"506"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CIRC_0068655 SILENCING AMELIORATES HYPOXIA-INDUCED HUMAN CARDIOMYOCYTE INJURY BY REGULATING APOPTOTIC AND INFLAMMATORY RESPONSES.","authors":"Ting You, Kang Peng, Jing Yi, Yafang Du, Peiyong Jiang, Dianmei Zeng, Ji Wu, Jian Liu, Songjiang Wu","doi":"10.1097/SHK.0000000000002504","DOIUrl":"10.1097/SHK.0000000000002504","url":null,"abstract":"<p><strong>Abstract: </strong>Background: There is growing evidence suggesting that the dysregulation of circular RNAs (circRNAs) plays a significant role in various myocardial disorders, including myocardial ischemia. This study aimed to explore the function of hsa_circ_0068655 (circ_0068655) in hypoxia-induced cardiomyocyte injury. Methods: Human AC16 cardiomyocyte cells were cultured under anaerobic condition to induce an in vitro model of myocardial ischemia. Cell apoptosis was assessed by Annexin V-fluorescein isothiocyanate staining and caspase-3 and caspase-9 activity assays. Cell proliferation was analyzed by 5-ethynyl-2'-deoxyuridine incorporation assay. Inflammation was evaluated by enzyme-linked immunosorbent assays. Circ_0068655, miR-370-3p, and BCL-2-like 11 (BCL2L11) expression were detected by real-time quantitative polymerase chain reaction or western blotting. The target interactions among circ_0068655, miR-370-3p, and BCL2L11 were predicted using bioinformatics tools and validated using dual-luciferase reporter assays and RNA immunoprecipitation assays. Results: Hypoxia treatment led to upregulated expression of circ_0068655 and BCL2L11, and downregulated expression of miR-370-3p in AC16 cells. This treatment also resulted in reduced cell viability, increased apoptosis rate, elevated caspase-9/3 activities and cleavage, and enhanced production of TNF-α, IL-6, and IL-1β. Notably, knockdown of circ_0068655 alleviated these detrimental effects. In addition, circ_0068655 silencing-mediated effects were restored by decreasing miR-370-3p expression in hypoxia-treated AC16 cells. Moreover, ectopic BCL2L11 expression remitted the effects of miR-370-3p overexpression on hypoxia-treated AC16 cells. Mechanistically, circ_0068655 was found to act as a sponge for miR-370-3p, thereby regulating BCL2L11 expression. Conclusion: Circ_0068655 silencing ameliorated hypoxia-induced human cardiomyocyte injury through the miR-370-3p/BCL2L11 axis.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"390-398"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ETANERCEPT REDUCES ACUTE TISSUE INJURY AND MORTALITY ASSOCIATED TO ZYMOSAN-INDUCED MULTIPLE ORGAN DYSFUNCTION SYNDROME SHOCK (2008) DOI:10.1097/SHK.0B013E3181507234, PMID: 17724436.","authors":"Giuseppe Malleo, Emanuela Mazzon, Tiziana Genovese, Rosanna Di Paola, Carmelo Muià, Rocco Caminiti, Emanuela Esposito, Paolo Di Bella, Salvatore Cuzzocrea","doi":"10.1097/SHK.0000000000002520","DOIUrl":"10.1097/SHK.0000000000002520","url":null,"abstract":"","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":"63 3","pages":"503"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RESPIRATORY VARIATION OF VELOCITY TIME INTEGRAL AND PEAK VELOCITY OF LEFT VENTRICULAR OUTFLOW TRACT FOR PREDICTING HYPOTENSION AFTER INDUCTION OF GENERAL ANESTHESIA IN ELDERLY PATIENTS.","authors":"Jingjie Wan, Xiaofei Jin, Jun Chen, Ke Peng, Jin Xie","doi":"10.1097/SHK.0000000000002509","DOIUrl":"10.1097/SHK.0000000000002509","url":null,"abstract":"<p><strong>Abstract: </strong>Background : Hypotension after induction of general anesthesia may lead to severe complications in elderly patients. This study investigated whether the respiratory variation of velocity time integral (ΔVTI) and peak velocity (ΔVpeak) of left ventricular outflow tract (LVOT) could predict hypotension after induction of general anesthesia in elderly patients. Methods : 120 elderly patients undergoing selective operation under general anesthesia were enrolled in this study. ΔVTI and ΔVpeak of LVOT were measured by transthoracic echocardiography before induction of general anesthesia. After induction, mean arterial pressure (MAP) was recorded every 1 min for 15 min. Hypotension was defined as a decrease of more than 30% in MAP at baseline or MAP below 65 mmHg from the start of induction. Receiver operating characteristic curves with gray zone and multivariate logistic regression analysis were used to assess the ability of ΔVTI and ΔVpeak of LVOT to predict hypotension after induction of general anesthesia. Results : Hypotension occurred in 64 (53.3%) patients after induction of general anesthesia. The area under receiver operating characteristic curves (AUC) for δVpeak of LVOT to predict hypotension after induction of general anesthesia was 0.811, and the optimal cutoff value was 13.1% with a gray zone of 9.9% to 13.8%, including 45.0% of patients. The AUC for ΔVTI of LVOT was 0.890, and the optimal cutoff value was 13.8% with a gray zone of 11.1% to 13.9%, including 25.8% of patients. After adjusting for confounders, ΔVTI (Odds ratio = 2.24) and ΔVpeak (Odds ratio = 2.09) of LVOT were two significant independent predictors of hypotension after induction of general anesthesia. Conclusions : ΔVTI of LVOT was a reliable predictor of hypotension after the induction of general anesthesia in elderly patients. ΔVpeak of LVOT should be used cautiously to predict hypotension after induction of general anesthesia due to nearly half of elderly patients in the gray zone. Trial registration : This study was registered in the Chinese Clinical Trial Registry (registration number: ChiCTR2300077117).</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"411-416"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDENTIFICATION AND VERIFICATION OF FEATURE BIOMARKERS ASSOCIATED WITH CHOLINE METABOLISM IN SEPSIS-INDUCED CARDIOMYOPATHY.","authors":"Meng-Qin Pei, Zhen-Dong Sun, Yu-Shen Yang, Yu-Ming Fang, Ya-Fen Zeng, He-Fan He","doi":"10.1097/SHK.0000000000002513","DOIUrl":"10.1097/SHK.0000000000002513","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Sepsis-induced cardiomyopathy ( SIC ), one of the most common complications of sepsis, seriously affects the prognosis of critically ill patients. Choline metabolism is an important biological process in the organism, and the mechanism of its interaction with SIC is unclear. The aim of this study was to reveal the choline metabolism genes (CMGs) associated with SIC and to provide effective targets for the treatment of SIC . Methods: Through a comprehensive analysis of the microarray dataset GSE79962 (comprising 20 SIC patients and 11 healthy controls) from the GEO database, suspected co-expression modules and differentially expressed genes (DEGs) in SIC were identified. Hub CMGs were obtained by intersecting choline metabolism database with DEGs and key model genes. Afterward, hub CMGs most significantly involved in prognosis were further analyzed for the verification of major pathways of enrichment analysis. Finally, the expression of hub CMGs in in vivo and in vitro SIC model was verified by immunohistochemistry staining and quantitative real-time polymerase chain reaction analysis (qPCR). Results: Weighted gene co-expression network analysis identified 1 hub gene panel and 3,867 hub genes, which were intersected with DEGs and CMGs to obtain the same 3 hub CMGs:HIF-1α, DGKD, and PIK3R1. Only HIF-1α shows significant association with mortality ( P = 0.009). Subsequent differential analysis based on the high and low HIF-1α expression yielded 63 DEGs and then they were uploaded into Cytoscape software to construct a protein-protein interaction network and 6 hub genes with the highest priority were obtained (CISH, THBS1, IMP1, MYC, SOCS3, and VCAN). Finally, a multifactorial COX analysis revealed a significant correlation between HIF-1α and survival in SIC patients, which was further validated by in vitro and in vivo experiments. Conclusion: Our findings will provide new insights into the pathogenesis of SIC , and HIF-1α may have important applications as a potential biomarker for early detection and therapeutic intervention in SIC .</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"456-465"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OZONE THERAPY AMELIORATES LPS-INDUCED ACUTE LUNG INJURY IN MICE BY INHIBITING THE NLRP3/ASC/CASPASE-1 AXIS.","authors":"PengCheng Wang, QinYao Zhao, XiaoFang Zhu, ShuangJiao Cao, John P Williams, Jianxiong An","doi":"10.1097/SHK.0000000000002525","DOIUrl":"10.1097/SHK.0000000000002525","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Acute lung injury (ALI) is a common respiratory emergency with high incidence and mortality. Among its main pathologic mechanisms is the rapid and intense inflammatory response. Ozone is a naturally occurring compound and is known for its properties as an oxidizing agent. Ozone therapy is the clinical application of a mixture of ozone (O 3 ) and oxygen, used within nontoxic, safe concentrations. It could be used for the treatment of several diseases. Ozone rectal insufflation (O 3 -RI) is a treatment in which medical O 3 is introduced into the rectum to treat and prevent disease. Although O 3 therapy exerts anti-inflammatory effects, its function in ALI remains unclear. The aim of this study was to preliminarily investigate the role and function of O 3 -RI in ALI. Methods: A mouse model of ALI was established by intratracheal administration of LPS. O 3 -RI was administered 4 h following the modeling procedure. Lung histopathology, lung wet/dry ratio, protein content in bronchoalveolar lavage fluid (BALF), and myeloperoxidase activity in lung tissues, as well as the number of inflammatory cells and inflammatory cytokines in BALF, were assessed. The expression levels of NOD-like receptor thermal protein domain associated protein (NLRP3)/apoptosis-associated speck-like protein (ASC)/caspase-1 axis-related proteins in lung tissues were examined by real-time fluorescence quantitative polymerase chain reaction and Western blotting. Results: Ozone therapy reduced the wet/dry ratio of lung tissue and total protein content in BALF and attenuated lung edema and microvascular leakage in ALI mice. Ozone therapy reduced the myeloperoxidase content in the lung tissue, the number of inflammatory cells, and the content of inflammatory cytokines in BALF and attenuated lung tissue inflammation in mice with ALI. Ozone therapy ameliorated lung tissue morphological damage in ALI mice. Ozone therapy downregulated the expression of NLRP3/ASC/caspase-1 axis-related proteins. Conclusion: Ozone therapy attenuated LPS-induced ALI in mice, possibly by inhibiting NLRP3/ASC/caspase-1 axis. Ozone therapy is a valuable potential therapeutic modality for ALI.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"487-494"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142786993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FRAIL PARTICIPANTS IN RANDOMIZED CONTROLLED TRIALS OF ACUTE RESPIRATORY DISTRESS SYNDROME.","authors":"Theodora K Ntaidou, Vassilis G Giannakoulis, Eleni Papoutsi, Eleni A Vavouraki, Evangelia Theodorou, Georgios Papathanakos, Ioanna Dimopoulou, Christina Routsi, Anastasia Kotanidou, Ilias I Siempos","doi":"10.1097/SHK.0000000000002517","DOIUrl":"10.1097/SHK.0000000000002517","url":null,"abstract":"<p><strong>Abstract: </strong>Purpose: Observational studies showed that frailty is common in the intensive care unit and associated with poor outcomes. However, relevant data from interventional trials are scarce, and it is unknown whether outcomes improved over time. We endeavored to estimate temporal trends of representation and outcomes of frail participants in randomized controlled trials of acute respiratory distress syndrome (ARDS). Methods: We performed a secondary analysis of five ARDS Network and PETAL Network trials published between 2006 and 2019. Based on requirement for everyday assistance prior to hospitalization, we categorized participants into frail versus nonfrail. Results : Out of 3,630 participants with ARDS, 701 (19.3%) were frail. Representation of frail participants increased over time ( P = 0.001), while mortality remained stable ( P = 0.403) and as high as 39.4%. A total of 60.6% of frail participants were younger than 65 years old. Frailty was independently associated with 90-day mortality (odds ratio 1.62, 95% confidence interval 1.34-1.96, P < 0.001). Frail had fewer ventilator-free days and were more likely to have subsequent disability than nonfrail participants. Conclusion: In trials of ARDS, representation of frail participants increased, while their mortality did not improve over time. The ever-increasing vulnerable group of frail participants should be taken into consideration in the design of trials.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"435-440"},"PeriodicalIF":2.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}