Shock (Augusta, Ga.)最新文献

{"title":"Outcomes Associated With Norepinephrine Use Among Cardiac Intensive Care Unit Patients with Severe Shock.","authors":"Barry Burstein,&nbsp;Saraschandra Vallabhajosyula,&nbsp;Bradley Ternus,&nbsp;Dennis Murphree,&nbsp;Gregory W Barsness,&nbsp;Kianoush Kashani,&nbsp;Jacob C Jentzer","doi":"10.1097/SHK.0000000000001767","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001767","url":null,"abstract":"<p><strong>Background: </strong>Recent data suggests improved outcomes among cardiac intensive care unit (CICU) patients treated with norepinephrine, especially patients with severe shock. We aimed to describe the association between norepinephrine and mortality in CICU patients with severe shock, defined as those requiring high-dose vasopressors (HDV).</p><p><strong>Materials and results: </strong>We retrospectively evaluated Mayo Clinic CICU patients treated with vasopressors from 2007 to 2015. HDV was defined as a peak Cumulative Vasopressor Index of four for any vasopressor. Peak norepinephrine equivalent (NEE) dose was used to compare vasopressor doses. Multivariable logistic regression was used to determine predictors of hospital mortality.</p><p><strong>Results: </strong>We included 2,090 patients with a median age of 69 years (IQR 59-78), including 35% females; 44% of patients received HDV. Hospital mortality was higher among patients receiving HDV (42% vs. 16%, unadjusted OR 3.87, 95% CI 3.16-4.75, P < 0.01). On multivariable analysis in HDV patients, hospital mortality increased with rising peak NEE (adjusted OR 1.02 per 0.01 mcg/kg/min, 95% CI 1.01-1.02, P  < 0.01) and the use of NE was associated with lower hospital mortality (adjusted OR 0.46, 95% CI 0.31-0.72, P < 0.01). After adjustment for illness severity, peak NEE and norepinephrine use were not associated with mortality among patients who did not require HDV.</p><p><strong>Conclusions: </strong>Mortality is high among CICU patients requiring HDV, and rises with increasing vasopressor requirements. Use of NE was associated with lower mortality among patients requiring HDV, but not among those without HDV, implying that patients with more severe shock may benefit from preferential use of NE.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"522-528"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39418962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhalation of 2% Hydrogen Improves Survival Rate and Attenuates Shedding of Vascular Endothelial Glycocalyx in Rats with Heat Stroke.","authors":"Sang Kien Truong,&nbsp;Takasumi Katoh,&nbsp;Soichiro Mimuro,&nbsp;Tsunehisa Sato,&nbsp;Kensuke Kobayashi,&nbsp;Yoshiki Nakajima","doi":"10.1097/SHK.0000000000001797","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001797","url":null,"abstract":"<p><strong>Abstract: </strong>Heat stroke is characterized by excessive oxidative stress and inflammatory responses, both of which are implicated in vascular endothelial glycocalyx shedding and heat-stroke mortality. Although molecular hydrogen has antioxidation and anti-inflammatory potency, its effect on the vascular endothelial glycocalyx in heat stroke has not been examined. Therefore, the aim of this study was to investigate the influence of hydrogen inhalation on the survival and thickness of the vascular endothelial glycocalyx of rats subjected to heat stroke. Altogether, 98 Wistar rats were assigned to the experiments. A heat-controlled chamber set at 40°C temperature and 60% humidity was used to induce heat stroke. After preparation, the anesthetized rats that underwent the heating process were subjected to an hour of stabilization in which 0%, 2%, or 4% hydrogen gas was inhaled and maintained until the experiment ended. In addition to survival rate assessments, blood samples and left ventricles were collected to evaluate the thickness of the vascular endothelial glycocalyx and relevant biomarkers. The results showed that 2% hydrogen gas significantly improved survival in the heat-stroked rats and partially preserved the thickness of the endothelial glycocalyx. In addition, serum levels of endotoxin, syndecan-1, malondialdehyde, and tumor necrosis factor-α decreased, whereas superoxide dismutase levels increased, indicating that inhalation of 2% hydrogen attenuated the damage to the vascular endothelial glycocalyx through its antioxidative and anti-inflammatory effects.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"593-600"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39418963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incidence and Impact of Dysglycemia in Patients with Sepsis Under Moderate Glycemic Control.","authors":"Seitaro Fujishima,&nbsp;Satoshi Gando,&nbsp;Daizoh Saitoh,&nbsp;Shigeki Kushimoto,&nbsp;Hiroshi Ogura,&nbsp;Toshikazu Abe,&nbsp;Atsushi Shiraishi,&nbsp;Toshihiko Mayumi,&nbsp;Junichi Sasaki,&nbsp;Joji Kotani,&nbsp;Naoshi Takeyama,&nbsp;Ryosuke Tsuruta,&nbsp;Kiyotsugu Takuma,&nbsp;Norio Yamashita,&nbsp;Shin-Ichiro Shiraishi,&nbsp;Hiroto Ikeda,&nbsp;Yasukazu Shiino,&nbsp;Takehiko Tarui,&nbsp;Taka-Aki Nakada,&nbsp;Toru Hifumi,&nbsp;Yasuhiro Otomo,&nbsp;Kohji Okamoto,&nbsp;Yuichiro Sakamoto,&nbsp;Akiyoshi Hagiwara,&nbsp;Tomohiko Masuno,&nbsp;Masashi Ueyama,&nbsp;Satoshi Fujimi,&nbsp;Kazuma Yamakawa,&nbsp;Yutaka Umemura","doi":"10.1097/SHK.0000000000001794","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001794","url":null,"abstract":"<p><strong>Abstract: </strong>Glycemic control strategies for sepsis have changed significantly over the last decade, but their impact on dysglycemia and its associated outcomes has been poorly understood. In addition, there is controversy regarding the detrimental effects of hyperglycemia in sepsis. To evaluate the incidence and risks of dysglycemia under current strategy, we conducted a preplanned subanalysis of the sepsis cohort in a prospective, multicenter FORECAST study. A total of 1,140 patients with severe sepsis, including 259 patients with pre-existing diabetes, were included. Median blood glucose levels were approximately 140 mg/dL at 0 and 72 h indicating that blood glucose was moderately controlled. The rate of initial and late hyperglycemia was 27.3% and 21.7%, respectively. The rate of early hypoglycemic episodes during the initial 24 h was 13.2%. Glycemic control was accompanied by a higher percentage of initial and late hyperglycemia but not with early hypoglycemic episodes, suggesting that glycemic control was targeted at excess hyperglycemia. In nondiabetic patients, late hyperglycemia (hazard ratio, 95% confidence interval; P value: 1.816, 1.116-2.955, 0.016) and early hypoglycemic episodes (1.936, 1.180-3.175, 0.009) were positively associated with in-hospital mortality. Further subgroup analysis suggested that late hyperglycemia and early hypoglycemic episodes independently, and probably synergistically, affect the outcomes. In diabetic patients, however, these correlations were not observed. In conclusion, a significantly high incidence of dysglycemia was observed in our sepsis cohort under moderate glycemic control. Late hyperglycemia in addition to early hypoglycemia was associated with poor outcomes at least in nondiabetic patients. More sophisticated approaches are necessary to reduce the incidence of these serious complications.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"507-513"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38891740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Levosimendan Ameliorates Post-resuscitation Acute Intestinal Microcirculation Dysfunction Partly Independent of its Effects on Systemic Circulation: A Pilot Study on Cardiac Arrest in a Rat Model.","authors":"Tianyuan Jia,&nbsp;Shiwei Wang,&nbsp;Chengzhun Luo,&nbsp;Zida Wang,&nbsp;Guoxiang Liu,&nbsp;Zhaoming Shang,&nbsp;Xiaoye Lu,&nbsp;Qian Yang,&nbsp;Changqing Zhu","doi":"10.1097/SHK.0000000000001771","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001771","url":null,"abstract":"<p><strong>Background: </strong>Cardiac arrest (CA) is recognized as a life-threatening disease; however, the initial resuscitation success rate has increased due to advances in clinical treatment. Levosimendan has shown potential benefits in CA patients. However, its exact function on intestinal and systemic circulation in CA or post-cardiac arrest syndrome (PCAS) remained unclear. This study preliminarily investigated the link between dynamic changes in intestine and systemic hemodynamics post-resuscitation after levosimendan administration.</p><p><strong>Methods: </strong>Twenty-five rats were randomized into three groups: sham control group (n = 5), levosimendan group (n = 10), and vehicle group (n = 10). Intestinal microcirculation was observed using a sidestream dark-field imaging device at baseline and each hour of the return of spontaneous circulation (≤6 h). Systemic hemodynamics, serum indicators of cardiac injury, and tissue perfusion/metabolism were measured by echo-cardiography, a biological signal acquisition system, and an enzyme-linked immunosorbent assay, respectively.</p><p><strong>Results: </strong>Myocardial injury and global and intestinal perfusion/metabolism were significantly improved by levosimendan treatment. There was no statistically significant difference in the mean arterial pressure values between the vehicle and levosimendan groups (P > 0.05). The intestinal and systemic circulation measurements showed poor correlation (Pearson r-value of variable combinations in the levosimendan group was much less than 0.75; P < 0.01, levosimendan vs. vehicle group).</p><p><strong>Conclusions: </strong>Levosimendan significantly reduced the cardiac injury and corrected the metabolic status in an experimental rat model of ventricular fibrillation induced CA and cardiopulmonary resuscitation. Levosimendan may ameliorate PCAS-induced intestinal microcirculation dysfunction, partly independent of its effects on macrocirculation.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"639-646"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25468946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of NF-κB1 and the Non-canonical NF-κB Signaling Pathway in the Pathogenesis of Acute Kidney Injury in Shiga-toxin-2-induced Hemolytic-uremic Syndrome in Mice.","authors":"Isabelle V Sobbe,&nbsp;Nadine Krieg,&nbsp;Sophie Dennhardt,&nbsp;Sina M Coldewey","doi":"10.1097/SHK.0000000000001558","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001558","url":null,"abstract":"<p><strong>Abstract: </strong>The hemolytic-uremic syndrome (HUS) is a thrombotic microangiopathy which can occur as a severe systemic complication after an infection with Shiga-toxin-(Stx)-producing Escherichia coli (STEC). Elevated levels of proinflammatory cytokines associated with the classical nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) signaling pathway were detected in the urine of HUS patients. Thus, we hypothesize that the immune response of the infected organism triggered by Stx can affect the kidneys and contributes to acute kidney injury. Hitherto, the role of the classical and non-canonical NF-κB signaling pathway in HUS has not been evaluated systematically in vivo. We aimed to investigate in a murine model of Shiga toxin-induced HUS-like disease, whether one or both pathways are involved in the renal pathology in HUS. In kidneys of mice subjected to Stx or sham-treated mice, protein or gene expression analyses were performed to assess the expression of receptors activating the classical and non-canonical pathway, such as Fn14 and CD40, levels of NF-κB1/RelA and NF-κB2/RelB including its upstream signaling proteins, and expression of cytokines as target molecules of both pathways. In line with a higher expression of Fn14 and CD40, we detected an enhanced translocation of NF-κB1 and RelA as well as NF-κB2 and RelB into the nucleus accompanied by an increased gene expression of the NF-κB1-target cytokines Ccl20, Cxcl2, Ccl2, Cxcl1, IL-6, TNF-α, Cxcl10, and Ccl5, indicating an activation of the classical and non-canonical NF-κB pathway. Thereby, we provide, for the first time, in vivo evidence for an involvement of both NF-κB signaling pathways in renal pathophysiology of STEC-HUS.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"573-581"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37958849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Plasma Levels of Fas Ligand with Severity and Outcome of Sepsis.","authors":"Hongseok Yoo,&nbsp;Jin Young Lee,&nbsp;Junseon Park,&nbsp;Gee Young Suh,&nbsp;Kyeongman Jeon","doi":"10.1097/SHK.0000000000001753","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001753","url":null,"abstract":"<p><strong>Introduction: </strong>Levels of the apoptosis regulator Fas ligand (FasL) are associated with severity of sepsis, but its association with the mortality of sepsis and necroptosis, a regulated cell death mechanism, is not yet clear. We aimed to assess the association of FasL level with outcomes of sepsis and receptor interacting protein kinase-3 (RIPK3), an essential necroptosis mediator, for determining the relationship between FasL and necroptosis.</p><p><strong>Methods: </strong>Plasma FasL and RIPK3 levels were measured by ELISA from prospectively enrolled critically ill adult patients. The best cut-off level of FasL for 28-day mortality prediction was determined by Youden's index. The association between plasma levels of FasL and RIPK3 was assessed by a linear regression method.</p><p><strong>Results: </strong>Among 188 patients, 58 (30.9%) were diagnosed with sepsis and 84 (44.7%) with septic shock, respectively. Plasma levels of FasL increased in the group order of control, sepsis, and septic shock groups (P for trend < 0.001). For 142 patients with sepsis, organ dysfunction and septic shock were more prevalent in the group with plasma FasL levels that were higher than the best cut-off level. A significant difference in mortality between high and low FasL patients was observed up to 90 days (Log-rank P = 0.013). FasL levels did not significantly change over day 3 and day 7. FasL levels were not correlated with those of RIPK3.</p><p><strong>Conclusions: </strong>The plasma level of FasL was associated with severity of sepsis and was predictive of mortality. However, it was not correlated with RIPK3 level.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"544-550"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25361532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations Between Elevated Systolic Blood Pressure and Outcomes in Critically Ill Patients: A Retrospective Cohort Study and Propensity Analysis.","authors":"An-Min Hu,&nbsp;Chao Hai,&nbsp;Hai-Bo Wang,&nbsp;Zhongheng Zhang,&nbsp;Ling-Bin Sun,&nbsp;Zhong-Jun Zhang,&nbsp;Hui-Ping Li","doi":"10.1097/SHK.0000000000001774","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001774","url":null,"abstract":"<p><strong>Introduction: </strong>Studies have shown nonlinear relationships between systolic blood pressure (SBP) and outcomes, with increased risk observed at both low and high blood pressure levels. However, the relationships between cumulative times at different SBP levels and outcomes in critically ill patients remain unclear. We hypothesized that an appropriate SBP level is associated with a decrease in adverse outcomes after intensive care unit (ICU) admission.</p><p><strong>Methods: </strong>This study was a retrospective analysis of data from the Medical Information Mart for Intensive Care (MIMIC) III database, which includes more than 1,000,000 SBP records from 12,820 patients. Associations of cumulative times at four SBP ranges (<100 mm Hg, 100-120 mm Hg, 120-140 mm Hg, and ≥140 mm Hg) with mortality (12-, 3-, 1-month mortality and in-hospital mortality) were evaluated. Restricted cubic splines and multivariable Cox regression models were employed to assess associations between mortality and cumulative times at SBP levels (4 levels: <2, 2-12, 12-36, and ≥36 h) over 72 h of ICU admission. Additionally, 120 mm Hg to 140 mm Hg was subdivided into <12 h (Group L) and ≥12 h (Group M) subsets and subjected to propensity-score matching and subgroup analyses.</p><p><strong>Results: </strong>At 120 mm Hg to 140 mm Hg, level-4 SBP was associated with lower adjusted risks of mortality at 12 months (OR, 0.71; CI, 0.61-0.81), 3 months (OR, 0.72; CI, 0.61-0.85), and 1 month (OR, 0.61; CI, 0.48-0.79) and in the hospital (OR, 0.71; CI, 0.58-0.88) than level-1 SBP. The cumulative times at the other 3 SBP ranges (<100 mm Hg, 100-120 mm Hg, and ≥140 mm Hg) were not independent risk predictors of prognosis. Furthermore, Group M had lower 12-month mortality than Group L, which remained in the propensity-score matched and subgroup analyses.</p><p><strong>Conclusions: </strong>SBP at 120 mm Hg to 140 mm Hg was associated with decreased adverse outcomes. Randomized trials are required to determine whether the outcomes in critically ill patients improve with early maintenance of a SBP level at 120 mm Hg to 140 mm Hg.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"557-563"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25520941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What's New in Shock, October 2021?","authors":"Hugo C Castro-Faria-Neto","doi":"10.1097/SHK.0000000000001857","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001857","url":null,"abstract":"","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"479-483"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39418961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MUC1 Mitigates Renal Injury and Inflammation in Endotoxin-Induced Acute Kidney Injury by Inhibiting the TLR4-MD2 Axis and Reducing Pro-inflammatory Macrophages Infiltration.","authors":"Jean-Baptiste Gibier,&nbsp;Thomas Swierczewski,&nbsp;Marie Csanyi,&nbsp;Brigitte Hemon,&nbsp;Francois Glowacki,&nbsp;Patrice Maboudou,&nbsp;Isabelle Van Seuningen,&nbsp;Christelle Cauffiez,&nbsp;Nicolas Pottier,&nbsp;Sebastien Aubert,&nbsp;Michael Perrais,&nbsp;Viviane Gnemmi","doi":"10.1097/SHK.0000000000001742","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001742","url":null,"abstract":"<p><strong>Abstract: </strong>Sepsis is the leading cause of acute kidney injury (AKI) in critical care patients. A cornerstone of sepsis-associated AKI is dysregulated inflammation driven by excessive activation of Toll-like receptor 4 (TLR4) pathway. MUC1, a membrane-bound mucin expressed in both epithelial tubular cells and renal macrophages, has been shown to be involved in the regulation of TLRs. Therefore, we hypothesized that MUC1 could mitigate the renal inflammatory response to TLR4 activation. To test this hypothesis, we used a murine model of endotoxin-induced AKI by intraperitoneal injection of LPS. We showed that Muc1-/- mice have a more severe renal dysfunction, an increased activation of the tissular NF-kB pathway and secreted more pro inflammatory cytokines compare to Muc1+/+ mice. By flow cytometry, we observed that the proportion of M1 (pro-inflammatory) macrophages in the kidneys of Muc1-/- mice was significantly increased. In human and murine primary macrophages, we showed that MUC1 is only induced in M1 type macrophages and that macrophages derived from Muc1-/- mice secreted more pro-inflammatory cytokines. Eventually, in HEK293 cells, we showed that MUC1 cytosolic domain (CT) seems necessary for the negative regulation of TLR4 by proximity ligation assay, MUC1-CT is in close relationship with TLR4 and acts as a competitive inhibitor of the recruitment of MYD88. Overall our results support that in the context of endotoxin-induced AKI, MUC1 plays a significant role in controlling disease severity by regulating negatively the TLR4-MD2 axis.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"629-638"},"PeriodicalIF":3.1,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25327763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brief High Oxygen Concentration Induces Oxidative Stress in Leukocytes and Platelets: A Randomized Cross-over Pilot Study in Healthy Male Volunteers.","authors":"Christina Hafner,&nbsp;Sibylle Pramhas,&nbsp;Wolfgang Schaubmayr,&nbsp;Alice Assinger,&nbsp;Andreas Gleiss,&nbsp;Eva Verena Tretter,&nbsp;Klaus Ulrich Klein,&nbsp;Gisela Scharbert","doi":"10.1097/SHK.0000000000001728","DOIUrl":"https://doi.org/10.1097/SHK.0000000000001728","url":null,"abstract":"<p><strong>Background: </strong>Supplemental oxygen is administered routinely in the clinical setting to relieve or prevent tissue hypoxia, but excessive exposure may induce oxidative damage or disrupt essential homeostatic functions. It is speculated that oxidative stress in leukocytes and platelets may contribute to vascular diseases by promoting inflammation and cell aggregation.</p><p><strong>Methods: </strong>In this pilot study 30 healthy male volunteers (18-65 years) were exposed to high oxygen concentration (non-rebreather mask, 8 L/min, 100% O2) and synthetic air (non-rebreather mask, 8 L/min, 21% O2) in a cross-over design for 20 min at a 3-week interval. Venous blood samples were obtained at baseline and 1, 3, and 6 h postintervention. Primary outcome was generation of reactive oxygen species in leukocytes as measured by the redox-sensitive fluorescent dye dihydrorhodamine 123. Additional outcomes were oxidative stress in platelets and platelet aggregation as measured by thromboelastography (ROTEM) and Multiplate analyses.</p><p><strong>Findings: </strong>High oxygen exposure induced oxidative stress in leukocytes as evidenced by significantly higher mean fluorescence intensity (MFI) compared with synthetic air at 3 h postintervention (47% higher, P = 0.015) and 6 h postintervention (37% higher, P = 0.133). Oxidative stress was also detectable in platelets (33% higher MFI in comparison with synthetic air at 6 h, P = 0.024; MFI 20% above baseline at 3 h, P  = 0.036; 37% above baseline at 6 h, P = 0.002). ROTEM analyses demonstrated reduced mean clotting time 1 h postintervention compared with baseline (-4%, P = 0.049), whereas there were no significant effects on other surrogate coagulation parameters.</p><p><strong>Conclusion: </strong>Clinically relevant oxygen exposure induces oxidative stress in leukocytes and platelets, which may influence the immune and clotting functions of these cells.</p>","PeriodicalId":238832,"journal":{"name":"Shock (Augusta, Ga.)","volume":" ","pages":"384-395"},"PeriodicalIF":3.1,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25484850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}