Acute respiratory distress syndrome (ARDS) is a common respiratory emergency, but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures. Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS, but the application of hydrogen has flammable and explosive safety concerns. Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance, thus improving ARDS in patients and animal models. Coral calcium hydrogenation (CCH) is a new solid molecular hydrogen carrier prepared from coral calcium (CC). Whether and how CCH affects acute lung injury in ARDS remains unstudied. In this study, we observed the therapeutic effect of CCH on lipopolysaccharide (LPS) induced acute lung injury in ARDS mice. The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable, demonstrating a significant improvement compared to the untreated ARDS model group. CCH treatment significantly reduced pulmonary hemorrhage and edema, and improved pulmonary function and local microcirculation in ARDS mice. CCH promoted mitochondrial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2), improved lung mitochondrial dysfunction induced by LPS, and reduced oxidative stress damage. The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

Ciprofol (CIP) for procedural sedation and analgesia (PSA) for painless gastrointestinal endoscopy (GE) can cause respiratory or cardiovascular complications. The literature suggests that intravenous (IV) lidocaine infusion can alleviate visceral pain and enhance humans’ ventilator response to CO2. Therefore, it was hypothesized that IV lidocaine could reduce the CIP dose for painless GE and improve recovery time. This randomized placebo-controlled trial included 40 patients undergoing GE. After CIP titration for unconsciousness, patients in group L were given IV lidocaine (1.5 mg/kg bolus dose, then a 2 mg/kg/h continuous infusion); the same volume saline as placebo was given for N group patients. The primary endpoint was the required CIP dose. Secondary endpoints were: endoscopic examination time, awakening time, post-anesthesia care unit (PACU) discharge time, pain and fatigue after awakening, adverse events, and endoscopist’s and patient’s satisfaction. Both cohorts had comparable demographic characteristics. Group L’s CIP consumption was decreased by 23.0

Background Postoperative sore throat (POST) is an unpleasant outcome that can occur as a result of tracheal intubation in adults. Increased pressure from the endotracheal tube (ETT) cuff often leads to local mucosal injury, resulting in sore throat. The purpose of this study was to compare the effect of two different ETT cuff pressure monitoring systems vs. no cuff pressure monitoring on the incidence and severity of POST in adults. Methods One hundred and fourteen ASA I-III patients of either gender, aged 18–65 years, and undergoing surgery requiring endotracheal intubation were included in this study. Patients were randomized into three groups: control (C), cuff pressure gauge (G), and automated cuff controller (A). The ETT cuff pressure was not monitored intraoperatively in group C but was monitored using a cuff pressure gauge and an automated cuff controller in groups G and A, respectively. Postoperatively, patients were assessed at 2, 24, and 48 h for the presence and severity of POST, hoarseness and cough. Results One hundred and eleven patients completed the study. POST occurred in 40.5% of the patients in group G ( n = 37) ( p = 0.013) and 23.7% of the patients in group A ( n = 38) ( p < 0.001) within 48 h after surgery, compared to 69.4% in group C ( n = 36). There were no significant differences in hoarseness, coughing, and dysphagia across the groups at any time. When comparing groups A and C, individuals in group A exhibited a lower occurrence of significant (grade ≥ 2) POST and hoarseness (10.5% vs. 41.7%, p = 0.002; 26.3% vs. 58.3%, p = 0.005). The incidence of significant cough and dysphagia did not differ substantially across the patient groups within 48 h after surgery. POST scores in group A at 2, 24 h postoperatively were both 0 (0–0), which was significantly lower than those in group C (1 (0–2) at 2 h, p < 0.001 ; 1 (0–1) at 24 h, p = 0.001). POST in group G at 2 h postoperatively was graded as 0 (0–1.5) which was milder than group C ( P = 0.024). The severity of hoarseness in group A with scores of 0 (0–2) was superior to that in group C (2 (0–2), p = 0.006) at 2 h postoperatively. Conclusions In conclusion, the findings of this study indicated that the occurrence of POST can be reduced by using either the cuff pressure gauge approach or the automated cuff controller method. The automated cuff controller monitoring can potentially decrease the severity of POST and hoarseness. Trial registration Chinese Clinical Trial Registry, identifier: ChiCTR2100054089, Date: 08/12/2021.

Acute respiratory distress syndrome (ARDS) is an acute and severe clinical complication lacking effective therapeutic interventions. The disruption of the lung epithelial barrier plays a crucial role in ARDS pathogenesis. Recent studies have proposed the involvement of abnormal mitochondrial dynamics mediated by dynamin-related protein 1 (Drp1) in the mechanism of impaired epithelial barrier in ARDS. Hydrogen is an anti-oxidative stress molecule that regulates mitochondrial function via multiple signaling pathways. Our previous study confirmed that hydrogen modulated oxidative stress and attenuated acute pulmonary edema in ARDS by upregulating thioredoxin 1 (Trx1) expression, but the exact mechanism remains unclear. This study aimed to investigate the effects of hydrogen on mitochondrial dynamics both in vivo and in vitro. Our study revealed that hydrogen inhibited lipopolysaccharide (LPS)-induced phosphorylation of Drp1 (at Ser616), suppressed Drp1-mediated mitochondrial fission, alleviated epithelial tight junction damage and cell apoptosis, and improved the integrity of the epithelial barrier. This process was associated with the upregulation of Trx1 in lung epithelial tissues of ARDS mice by hydrogen. In addition, hydrogen treatment reduced the production of reactive oxygen species in LPS-induced airway epithelial cells (AECs) and increased the mitochondrial membrane potential, indicating that the mitochondrial dysfunction was restored. Then, the expression of tight junction proteins occludin and zonula occludens 1 was upregulated, and apoptosis in AECs was alleviated. Remarkably, the protective effects of hydrogen on the mitochondrial and epithelial barrier were eliminated after applying the Trx1 inhibitor PX-12. The results showed that hydrogen significantly inhibited the cell apoptosis and the disruption of epithelial tight junctions, maintaining the integrity of the epithelial barrier in mice of ARDS. This might be related to the inhibition of Drp1-mediated mitochondrial fission through the Trx1 pathway. The findings of this study provided a new theoretical basis for the application of hydrogen in the clinical treatment of ARDS.

Abstract Background Perioperative hypotension is frequently observed following the initiation of general anesthesia administration, often associated with adverse outcomes. This study assessed the effect of subclavian vein (SCV) diameter combined with perioperative fluid therapy on preventing post-induction hypotension (PIH) in patients with lower ASA status. Methods This two-part study included patients aged 18 to 65 years, classified as ASA physical status I or II, and scheduled for elective surgery. The first part (Part I) included 146 adult patients, where maximum SCV diameter (dSCVmax), minimum SCV diameter (dSCVmin), SCV collapsibility index (SCVCI) and SCV variability (SCVvariability) assessed using ultrasound. PIH was determined by reduction in mean arterial pressure (MAP) exceeding 30% from baseline measurement or any instance of MAP < falling below 65 mmHg for ≥ a duration of at least 1 min during the period from induction to 10 min after intubation. Receiver Operating Characteristic (ROC) curve analysis was employed to determine the predictive values of subclavian vein diameter and other relevant parameters. The second part comprised 124 adult patients, where patients with SCV diameter above the optimal cutoff value, as determined in Part I study, received 6 ml/kg of colloid solution within 20 min before induction. The study evaluated the impact of subclavian vein diameter combined with perioperative fluid therapy by comparing the observed incidence of PIH after induction of anesthesia. Results The areas under the curves (with 95% confidence intervals) for SCVCI and SCVvariability were both 0.819 (0.744–0.893). The optimal cutoff values were determined to be 45.4% and 14.7% (with sensitivity of 76.1% and specificity of 86.7%), respectively. Logistic regression analysis, after adjusting for confounding factors, demonstrated that both SCVCI and SCVvariability were significant predictors of PIH. A threshold of 45.4% for SCVCI was chosen as the grouping criterion. The incidence of PIH in patients receiving fluid therapy was significantly lower in the SCVCI ≥ 45.4% group compared to the SCVCI < 45.4% group. Conclusions Both SCVCI and SCVvariability are noninvasive parameters capable of predicting PIH, and their combination with perioperative fluid therapy can reduce the incidence of PIH.

Septic lung injury is characterized by uncontrollable inflammatory infiltrations and acute onset bilateral hypoxemia. Evidence has emerged of the beneficial effect of hydrogen in acute lung injury (ALI), but the underlying mechanism is unclear. In this research, the recovery action of hydrogen on lipopolysaccharide (LPS)-induced ALI in mice and A549 cells was investigated. The 7-day survival rate and body weight of mice were measured after intraperitoneal injection of LPS. Lung function was determined by a whole body plethysmography (WBP) system using the indicators respiratory rate and enhanced pause. Hematoxylin and eosin (HE) staining confirmed the signs of pulmonary edema and inflammatory ooze. Reverse transcription-polymerase chain reaction (RT-PCR) quantification was used to detect the expression of inflammatory factors. Western blotting analysis evaluated the expression levels of involved proteins in the AMP-activated protein kinase (AMPK) pathway. The experimental results confirmed that hydrogen provided an essential solution to the dissipative effects of LPS on survival rate, weight loss and lung function. The LPS-stimulated inflammatory factors, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were also suppressed by hydrogen in A549 cells. Western blot analysis showed that hydrogen significantly upregulated the levels of phosphorylated AMPK (p-AMPK) and lowered the LPS-induced increased expression of dynamin-related protein 1 (Drp1) and Caspase3. These findings prove that hydrogen attenuated LPS-treated ALI by activating the AMPK pathway, supporting the feasibility of hydrogen treatment for sepsis.

Objective:To investigate the protective effect of hydrogen on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in septic mice and the effect on the expression of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3)/tissue factor (TF) signaling pathway.Methods:A total of 64 male C57BL/6J mice were tested in two batches. According to the random number table method, mice in each batch were divided into four groups ( n=8): a control group (group C), a LPS group (group L), a LPS+ hydrogen group (group LH) and a hydrogen group (group H). Mice in groups C and H were intraperitoneally injected with normal saline at 10 ml/kg. Meanwhile, those in groups L and LH were intraperitoneally injected with 10 mg/kg LPS to establish an ALI model in septic mice. Groups C and L were conventionally housed for 12 h, while groups LH and H were inhaled with 4% hydrogen for 12 h. Then, 12 h after modeling, mice in batch 1 were used for lung histopathology, lung function tests and scattered Doppler flow imaging, while those in batch 2 were used for bronchoalveolar lavage and Western blot analysis. hematoxylin-eosin (H-E) staining was performed to observe lung histopathology and evaluate lung injury score. Whole-body plethysmography system was used to detect lung function indicators in mice: minute ventilation volume (MV), expiratory flow 50 (EF50), peak expiratory flow (PEF), and enhanced pause (Penh). Scattered Doppler flow imaging was conducted to detect blood flow in the right lung and the left hind foot of mice. The levels of NLRP3 inflammatory vesicles and TF in the lungs were measured by Western blot. The levels of inflammatory factors tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 in bronchoalveolar lavage fluid (BALF) of mice were detected by enzyme-linked immunosorbent assay (ELISA). Results:According to H-E staining, the lung tissue structure of mice in group C and group H was normal. The lung tissue structure of mice in group L was disorganized, with a large number of neutrophils infiltrating. The lung tissue of mice in group LH showed reduced neutrophils infiltrating and relieved edema. Compared with group C, the lung tissue damage score was significantly elevated in groups L and LH ( P<0.05). MV, EF50 and PEF were significantly declined, and Penh was significantly elevated (all P<0.05). Blood flow in the right lung and the left hindfoot significantly decreased ( P<0.05). The relative content of NLRP3 and TF in lung tissue significantly increased ( P<0.05). The concentrations of TNF-α and IL-6 in BALF significantly increased ( P<0.05). Compared with group C, there was no statistical differences in all indicators in group H ( P>0.05). Compared with group L, the lung tissue injury score of mice in group LH was significantly reduced ( P<0.05). MV and PEF significantly increased, Penh was significantly elevated (all P<0.05). The difference in EF50 was not statistically significant ( P>0.05). Blood flow in the right lung and the left hindfoot was significantly higher ( P<0.05). The relative content of NLRP3 and TF in lung tissue was significantly lower ( P<0.05). The concentrations of TNF-α and IL-6 in BALF were significantly lower ( P<0.05). Conclusions:Hydrogen alleviates LPS-induced ALI in septic mice, which may be related to inhibition of the NLRP3/TF expression and reduction of secretion of inflammatory factors by hydrogen.

目的 术后谵妄脑缺血、缺氧损伤相关.文中探讨脑氧饱和度(rScO2)监测在预测骨科高龄患者术后谵妄的应用价值.方法 回顾性分析2020年4-12月在南京市江宁医院行骨科下肢手术的高龄患者154例,年龄70～85岁.患者均于术前行认知状态(MMSE量表)和抑郁状态(GDS量表)评估.手术均采用全身麻醉联合脑电双频指数(BIS)、无创脑氧饱和度(rScO2)监测,且术中均行动脉血气监测.以静息状态和吸氧状态下的脑氧和动脉平均压均值记为基线值rScO2和MAP,并计算rScO2曲线下面积(AUC-rScO2);以动脉血气值计算脑氧摄取(CMRO2),并记录患者发生并发症以及恶心、呕吐等术后不良反应情况.采用logistic多元回归法分析谵妄相关危险因素.结果 154例患者中发生谵妄25例,谵妄发生率16.23％.谵妄患者术中rScO2最高值与基线值比较下降幅度均>30％.与非谵妄组比较,谵妄组患者rScO2下降幅度差异有统计学意义(12.1％vs 6.1％,P<0.05),术前与手术结束即刻血气分析结果差值△Glu(5.12 mol/L vs 2.12 mol/L,P<0.05)、△CMRO2(7.98％vs 4.02％,P<0.05)显著升高,差异有统计学意义.logistic多元回归统计结果提示,术后谵妄的危险因素包括高龄(OR=0.711,95％CI=0.029～1.443)、rScO2变异度(OR=0.331,95％CI=0.051～1.941)、CMRO2变异度(OR=0.407,95％CI=0.049～1.713)、糖尿病(OR=0.491,95％CI=0.027～1.740).结论 rScO2术中监测可预测高龄骨科下肢手术患者术后谵妄的发生,提示调整术中脑灌注,对减少高龄骨科患者术后谵妄发生有指导意义.