Aims: Seawater immersion significantly aggravated organ dysfunction following hemorrhagic shock, leading to higher mortality rate. However, the effective treatment is still unavailable in clinic. Mitochondria were involved in the onset and development of multiple organ function disorders; whether mitochondria participate in the cardiac dysfunction following seawater immersion combined with hemorrhagic shock remains poorly understood. Hence, we investigated the role and possible mechanism of mitochondria in seawater immersion combined with hemorrhage shock-induced cardiac dysfunction.Results: Mitochondrial fission protein dynamin-related protein 1 (Drp1) was activated and translocated from the cytoplasm to mitochondria in the heart following seawater immersion combined with hemorrhagic shock, leading to excessive mitochondrial fission. Excessive mitochondrial fission disrupted mitochondrial function and structure and activated mitophagy and apoptosis. At the same time, excessive mitochondrial fission resulted in disturbance of myocardial structure and hemodynamic disorders and ultimately provoked multiple organ dysfunction and high mortality. Further studies showed that the mitochondrial division inhibitor mitochondrial division inhibitor-1 can significantly reverse Drp1 mitochondrial translocation and inhibit mitochondrial fragmentation, reactive oxygen species (ROS) accumulation, mitophagy, and apoptosis and then protect circulation and vital organ functions, prolonging animal survival.Innovation: Our findings indicate that Drp1-mediated mitochondrial fission could be a novel therapeutic targets for the treatment of seawater immersion combined with hemorrhagic shock.Conclusion: Drp1 mitochondrial translocation played an important role in the cardiac dysfunction after seawater immersion combined with hemorrhage shock. Drp1-mediated excessive mitochondrial fission leads to cardiac dysfunction due to the mitochondrial structure and bioenergetics impairment.

Objective To observe the improved effect of propofol on vascular hyporeactivity in septic rats and its underlying mechanism. Methods A total of 96 SD rats (12 weeks old, both genders, weighing 200~220 g) were randomly divided into sham group (n=16), sepsis group (n=16, cecal ligation and puncture), propofol group (n=16), propofol+ROCK inhibitor Y-27632 group (n=16), propofol+PKCα inhibitor GO6976 group (n=16), propofol+IP3 inhibitor 2-APB group (n=8) and propofol+gap junction inhibitor metoclopramide sodium (Movens) group (n=8). In vitro vascular ring reactivity and vascular calcium sensitivity were measured to observe the improved effects of propofol on vascular hyporeactivity in septic rats and its relationships with RhoA/ROCK, PKCα, IP3 and cell gap junction. Results Determination of in vitro vascular ring and calcium sensitivity showed that the contractile reactivity to norepinephrine (NE) and to calcium sensitivity were significantly decreased in the arterial rings isolated from the septic rats compared with those from the sham group, with the dose-response curve shifting to the right, and most significant decrease by 51.42% in the superior mesenteric artery (SMA, P < 0.05). Propofol treatment significantly improved the hyporeactivity and calcium sensitivity of the vessels isolated from the septic rats, especially those of the femoral artery with a recovery rate of 89.57% (P < 0.05). In comparison with the propofol group, the dose-response curves of the propofol+Y-27632 group and the propofol+GO6976 group were shifting to right, indicating that Y-27632 and GO6976 could significantly inhibit the amelioration of propofol on calcium sensitivity of SMA in severely septic rats with an inhibitory rate of 146.95% and 88.63% (P < 0.05), respectively. Isolated vascular reactivity measurement demonstrated that Y-27632 and Movens treatment significantly antagonized the ameliorated role of propofol on hyporeactivity of blood vessels from the septic rats with an inhibitory rate of 40.79% and 169.90% (P < 0.05), separately, while no such effect was observed in the propofol+GO6976 and propofol+2-APB groups. Conclusion Propofol treatment can significantly improve vascular hyporeactivity of septic rats, which may attribute to the increase of vascular calcium sensitivity through RhoA/ROCK pathway.

Introduction: Marine casualties are increasing, and mortality from trauma associated with immersion in seawater is high. However, the associated pathophysiological characteristics remain unclear, limiting research into the early emergency treatment strategy. Methods: Healthy and 50% hemorrhagic shock rats were soaked in 15 degrees C and 21 degrees C seawater for 2 h, 4 h and 6 h, respectively, and the effects on vital signs, internal environment, tissue metabolism, lethal triad, vital organ functions and survival were observed.Results: Immersion in seawater can cause death in healthy rats. Rats with hemorrhagic shock in 15 degrees C seawater showed a lower survival rate than the corresponding groups in 21 degrees C seawater. Moreover, compared with 21 degrees C seawater, 15 degrees C seawater played a more remarkable role in decreasing mean arterial pressure, heart rate, and respiration rate, increasing water content and decreasing Na+/K+-ATPase activity in the brain and lung; increase in plasma osmolality, Na+, K+, Cl-, and the occurrence of the lethal triad manifested by a decrease in core body temperature, pH, lactate, and an increase in coagulation parameters, as well as damage to cardiac, intestinal, hepatic, and renal functions in rats with hemorrhagic shock. Conclusions: Immersion in seawater at low temperatures could be lethal to healthy rats, causing the occurrence of a lethal triad and damage to vital organs. Furthermore, 15 degrees C seawater had a more significant effect than 21 degrees C-seawater on aggravating the imbalance of internal environment and tissue metabolism, resulting in a higher incidence of the lethal triad and thus aggravating the dysfunctions of vital organs, which eventually resulted in higher mortality in rats with hemorrhagic shock.(c) 2022 Published by Elsevier Inc.

对负压隔离病房的空气环境以及病房内污染气体扩散机理进行了研究,利用数值模拟方法分析病房内流场、压力场、温度场和污染气体浓度场的整体分布,提出两个气流组织改进方案,优化病房污染气体扩散控制效果.模拟结果表明,三种通风方案均能保证不同区域之间满足大于5 Pa的压力梯度,病房温度分布满足夏季室内空调温度设计要求,采用顶送风/病床上方布置排风口的气流组织,能保证病房达到病患舒适度,并且能有效控制污染气体扩散.

目的 观察抗氧化干预对低氧低糖处理后血管平滑肌细胞(VSMC)自噬和铁死亡发生的影响及其与血管功能的关系.方法 采用低氧低糖培养的VSMC和创伤失血休克大鼠模型,观察抗氧化剂依达拉奉(EDA)对低氧低糖处理后VSMC中自噬标志物、铁死亡标志物及细胞反应性的影响,并观察EDA对休克大鼠血管反应性的影响.结果 低氧低糖处理后VSMC中自噬标志物LC3-Ⅱ/LC3-Ⅰ比值升高、p62蛋白表达水平降低,提示自噬水平升高.低氧低糖也导致了VSMC铁死亡的发生,铁死亡标志物谷胱甘肽过氧化物酶4(GPx4)和溶质载体家族7成员11(SLC7A11)的表达水平降低.抗氧化剂EDA处理可抑制细胞自噬水平的升高,使LC3-Ⅱ/LC3-Ⅰ比值降低、p62蛋白表达水平升高;但EDA对GPx4和SLC7A11表达的影响无统计学意义.同时,低氧低糖处理后细胞收缩反应性明显降低,EDA处理可恢复低氧低糖细胞的收缩反应性.在创伤失血休克大鼠中,血管收缩反应性明显降低,抗氧化剂EDA处理可提高休克大鼠的血管收缩反应性.结论 抗氧化干预可抑制低氧低糖诱导的VSMC自噬,改善低氧细胞和休克血管的收缩功能.

Human haptoglobin (Hp) 1–1 is a potential protein drug to eliminate toxic effects of free hemoglobin, however it was difficult to selectively purify Hp 1–1 from pooled plasma. In this work, a specific purification process of Hp 1–1 from pooled human plasma was introduced, with PEG precipitation as the key step. First, frozen human plasma was thawed on ice to remove condensed proteins, then Hp 1–1, Hp 2–1 and Hp 2–2 were all precipitated by ammonium sulfate between 40%–65% (0 °C) saturation. 50% (m/v) PEG4000 solution (dissolved in 0.2 M HAc-NaAc pH 5.0) was then added into the pellet resuspension, and Hp 2–1, Hp 2–2 were precipitated between the concentration of 6%–15% (m/v) while Hp 1–1 remained in the 15% supernatant. The purity of Hp 1–1 raised from < 5% to a maximum of 50% after this step. Finally, Hp 1–1 with a maximum purity of > 98% was prepared after refined purification including anion exchange chromatography and hydrophobic chromatography. This process has a total Hp 1–1 recovery of 76.97%, along with characteristics of low cost, high efficiency, and high output, making it a process applicable for large-scale purification of Hp 1–1 from human plasma.

ABSTRACT Background: Hemorrhagic shock is the important factor for causing death of trauma and war injuries. However, pathophysiological characteristics and underlying mechanism in hemorrhagic shock with hot environment remain unclear. Methods: Hemorrhagic shock in hot environment rat model was used to explore the changes of mitochondrial and vital organ functions, the variation of the internal environment, stress factors, and inflammatory factors; meanwhile, the suitable treatment was further studied. Results: Above 36°C hot environment induced the increase of core temperature of rats, and the core temperature was not increased in 34°C hot environment, but the 34°C hot environment aggravated significantly hemorrhagic shock induced mortality. Further study showed that the mitochondrial functions of heart, liver, and kidney were more damaged in hemorrhagic shock rats with 34°C hot environment as compared with room environment. Moreover, the results showed that in hemorrhagic shock rats with hot environment, the blood concentration of Na+, K+, and plasma osmotic pressure, the expression of inflammatory factors tumor necrosis factor-α and interleukin-6 in the serum, as well as the stress factors Adrenocorticotropic Hormone and Glucocorticoid were all notably enhanced; and acidosis was more serous; oxygen supply and oxygen consumption were remarkably decreased. In addition, the present study demonstrated that mild hypothermia (10°C) fluid resuscitation could significantly improve the survival rate in hemorrhagic shock rats with hot environment as compared with normal temperature fluid resuscitation. Conclusions: Hot environment accelerated the death of hemorrhagic shock rats, which was related to the disorder of internal environment, the increase of inflammatory and stress factors. Furthermore, moderate hypothermic (10°C) fluid resuscitation was suitable for the treatment of hemorrhagic shock in hot environment.

Hypotension resuscitation is an important principle for the treatment after trauma. Current hypotensive resuscitation strategies cannot obtain an ideal outcome for remote regions. With the uncontrolled hemorrhagic shock (UHS) model in rats, the effects of norepinephrine (NE) on the tolerance time of hypotensive resuscitation, blood loss, vital organ functions, and animal survival were observed. Before bleeding was controlled, only the LR infusion could effectively maintain the MAP to 50–60 mmHg for 1 h, while the MAP gradually decreased with prolonging time, even with increasing infusion volume. Low-dose NE during hypotensive resuscitation prolonged the hypotensive tolerance time to 2–3 h, and the effect of 0.3 μg/kg/min NE was the best. Further studies showed that 0.3 μg/kg/min NE during hypotensive resuscitation significantly lightened the damage of organ function induced by UHS via protecting mitochondrial function, while the LR infusion did not. At the same time, NE administration improved Hb content, DO2, and VO2, and restored liver and kidney blood flow. The survival results showed that low-dose NE administration increased the survival rate and prolonged the survival time. Together, low-dose NE during hypotensive resuscitation was suitable for the early treatment of UHS, which can strive for the golden window of emergency treatment for serious trauma patients by reducing blood loss and protecting vital organ functions.

Vascular hyperpermeability is a complication of hemorrhagic shock. Pericytes (PCs) are a group of mural cells surrounded by microvessels that are located on the basolateral side of the endothelium. Previous studies have shown that damage to PCs contributes to the occurrence of many diseases such as diabetic retinopathy and myocardial infarction. Whether PCs can protect the vascular barrier function following hemorrhagic shock and the underlying mechanisms are unknown. A hemorrhagic shock rat model, Cx43 vascular endothelial cell (VEC)-specific knockdown mice, and VECs were used to investigate the role of PCs in vascular barrier function and their relationship with Cx43. The results showed that following hemorrhagic shock, the number of PCs in the microvessels was significantly decreased and was negatively associated with an increase in pulmonary and mesenteric vascular permeability. Exogenous infusion of PCs (10 6 cells per rat) colonized the microvessels and improved pulmonary and mesenteric vascular barrier function. Upregulation of Cx43 in PCs significantly increased the number of PCs colonizing the pulmonary vessels. In contrast, downregulation of Cx43 expression in PCs or knockout of Cx43 in VECs (Cx43 KO mice) significantly reduced PC colonization in pulmonary vessels in vivo and reduced direct contact formation between PCs and VECs in vitro . It has been suggested that PCs have an important protective effect on vascular barrier function in pulmonary and peripheral vessels following hemorrhagic shock. Cx43 plays an important role in the colonization of exogenous PCs in the microvessels. This finding provides a potential new shock treatment measure.

The cutting head of the single-stage impact sampler is used as the object.Using CFD technology,the flow field and particle trajectory inside the cutting head of two structures are numerical simulated.The nozzle is even with outer wall edge in model 1,and the nozzle end extends downward in model 2.The simulation results show that the mode2 is more effective than the model 1.Particles are more likely to break away from flow path and dash against on the capture surface.The ■number curve is steep.It can effectively capture the particles selectively by the size.The capture rate curve of the model 2 is steeper on the whole,and the cutting effect of particles is more ideal.The conclusion provides a certain technical reference for the design of the cutting head of a single-stage impact sampler.

BACKGROUND:Myocardial dysfunction played a vital role in organ damage after sepsis. Fluid resuscitation was the essential treatment in which Lactate Ringer's solution (LR) was commonly used. Since LR easily led to hyperlactatemia, its resuscitation effect was limited. Malate Ringer's solution (MR) was a new resuscitation crystal liquid. Whether MR had a protective effect on myocardial injury in sepsis and the relevant mechanism need to be studied. METHODS:The cecal ligation and puncture (CLP) inducing septic model and lipopolysaccharide (LPS) stimulating cardiomyocytes were used, and the cardiac function, the morphology and function of mitochondria were observed. The protective mechanism of MR on myocardial injury was explored by proteomics. Then the effects of TPP@PAMAM-MR, which consisted of the mitochondria- targeting polymer embodied malic acid, was further observed. RESULTS:Compared with LR, MR resuscitation significantly prolonged survival time, improved the cardiac function, alleviated the damages of liver, kidney and lung following sepsis in rats. The proteomics of myocardial tissue showed that differently expressed proteins between MR and LR infusion involved oxidative phosphorylation, apoptosis. Further study found that MR decreased ROS, improved the mitochondrial morphology and function, and ultimately enhanced mitochondrial respiration and promoted ATP production. Moreover, MR infusion decreased the expression of apoptosis-related proteins and increased the expression of anti-apoptotic proteins. TPP@PAMAM@MA was a polymer formed by wrapping L-malic acid with poly amido amine (PAMAM) modified triphenylphosphine material. TPP@PAMAM-MR (TPP-MR), which was synthesized by replacing the L-malic acid of MR with TPP@PAMAM@MA, was more efficient in targeting myocardial mitochondria and was superior to MR in protecting the sepsis-inducing myocardial injury. CONCLUSION:MR was suitable for protecting myocardial injury after sepsis. The mechanism was related to MR improving the function and morphology of cardiomyocyte mitochondria and inhibiting cardiomyocyte apoptosis. The protective effect of TPP-MR was superior to MR.

Chronic obstructive pulmonary disease (COPD) is a group of lung diseases characterized by limited airflow. COPD has many complications. COPD complicated with intestinal injury is one of the main complications. The aim of the present study was to reveal the material basis of COPD complicated with intestinal injury. 221 COPD patients were enrolled in this study. The metabolites in serum of COPD patients and healthy people were analyzed by ultra-high performance liquid chromatography (UPLC) and quadrupole time-of-flight mass spectrometry (TOF-MS). The role and mechanisms of the metabolic biomarkers from lung to intestine were investigated with xanthine oxidase (XO), heat shock protein 70 (HSP70) knockout mice, intestinal flora analysis and an isotopic tracking method. Hypoxanthine (Hyp) was identified one of the most significant changed metabolites in serum of COPD patients, it could shuttle from the lungs to intestine to mediate the intestine injury. Silence of or knocking out XO and HSP70 aggravated colon tissue injury of COPD. 15N13C labeled Hyp injected via trachea was detected in colon tissue. The possible mechanism of Hyp-mediated intestinal tissue injury was through HSP70/Nrf-2 signaling pathway. Hyp was an important biomarker of COPD patients, which can mediate the intestinal tissue injury. The mechanism was related to intestinal flora and HSP70/Nrf-2 signaling pathway. This finding provided a theoretical and experimental basis for COPD complicated with intestinal injury.Trial Registration Details: Clinical Trials: www.chictr.org.cn: chiCTR170019814Funding Information: This research was supported by National Natural Science Foundation of China (81400800).Declaration of Interests: The authors declare no conflict of interest.Ethics Approval Statement: WT mice (ICR, 6 weeks, 16-18g), xanthine oxidase (XO) KO mice (ICR, XO-/- , 6 weeks, 16-18g) and HSP70 (ICR, HSP70-/-, 6 weeks, 16-18g) were obtained from the Cyagen Biosciences Inc. and the ICR mice (8 weeks, 18-20 g) were obtained from Army Medical Center, Army Medical University, and the Affiliated Nanjing Hospital of Nanjing University of Chinese Medicine. All animal operations were approved by the Research Council and Animal Care and Use Committee of Animal Center of Army Medical Center, Army Medical University, and the Affiliated Nanjing Hospital of Nanjing University of Chinese Medicine. All patient experiments were performed under the guidance of the Helsinki Declaration and approved by the Research Council of Affiliated Nanjing Hospital of Nanjing University of Chinese Medicine (KY2017019).

Objective To investigate the protective effects of parthenolide (PTL) on intestinal barrier function in septic rats. Methods The septic model of rats was established by cecal ligation and puncture (CLP), and SD rats (200±20 g, male/female) were randomly divided into 6 groups: normal control (NC) group, sepsis (Sep) group, conventional treatment (LR) group (lactated Ringer's solution resuscitation+dopamine+cefuroxime sodium), and parthenolide (PTL) groups (1, 5 and 10 mg/kg parthenolide respectively on the basis of LR group). The changes of arterial blood pressure, survival rate and survival time of rats in each group were observed, and the optimal concentration of parthenolide in the treatment was determined. Moreover, the effects of parthenolide (at the optimal concentration) on the intestinal permeability, intestinal pathology, inflammatory cytokine levels, as well as liver and kidney functions in septic rats were further investigated. Results As compared with the NC group, the survival rate and survival time of septic rats were significantly decreased, so was the mean arterial pressure (MAP), while the levels of blood inflammatory cytokines were increased, and the liver and kidney functions were damaged. Conventional treatment improved the survival rate and survival time of septic rats to a certain extent, reduced the levels of inflammation cytokines and alleviated the liver and kidney damages. When compared with the LR group, the survival rates of 1, 5, and 10 mg/kg PTL groups were increased by 6.3%, 43.8%, and 18.8%, respectively, and the MAP in the PTL groups was elevated by 1.4%, 12.8%, and 7.1%, respectively, with those of 5 mg/kg PTL more significant. Further research found that PTL remarkably ameliorated the intestinal barrier function in septic rats, shown as a 55.1% reduction in the content of intestinal Evans blue (EB), a 69.5% decline in blood D-lactic acid concentration as compared with the LR group (P < 0.05), along with an improvement in intestinal epithelial structure, and a decrease in epithelial cell necrosis. In addition, PTL reduced the inflammatory cytokine levels greatly and improved the liver and kidney functions in septic rats. Conclusion PTL shows obvious protective effects on the intestinal barrier function of septic rats, and its mechanism may be related to the inhibition of septic inflammatory response.

Objective To investigate the protective effects of sterofundin on myocardial injury in septic rats. Methods A total of 280 SPF SD rats (half male and female, 12~14 weeks old, 200~220 g) were randomly divided into 4 groups: sham operation (Sham) group, sepsis (Sep) group, conventional treatment (Ct) group (with Ringer's lactate solution+dopamine+cefuroxime sodium), and malate ringer's solution (Mr) group (with sterofundin+dopamine+cefuroxime sodium). The rat model of sepsis was inflicted by cecal ligation and puncture (CLP). Subsequently, the effects of sterofundin treatment on the myocardial injury, cardiac output (CO), oxygen supply and consumption, liver and kidney perfusion, liver and kidney functions, survival time and survival rate of septic rats were observed. Results The cardiac output (CO), cardiac index (CI) and stroke index (SI) were significantly decreased in the Sep group, while the injuries were improved to some extent in the Ct group (P < 0.05). As compared with the Sep group, the improvement was more obvious in the Mr group, with CO, CI and SI values increased by 48.9%, 52.9% and 21.7% respectively, and the values were also greatly higher than those in the Ct group (P < 0.05). The mean arterial blood pressure was remarkably declined to about 70 mmHg in the Sep group, slightly improved to around 90 mmHg in the Ct group, and notably elevated in the Mr group by 43.2% when compared with the Sep group (P < 0.05). In addition, the liver and kidney functions were significantly ameliorated in the Mr group, along with decreased troponin T and lactate dehydrogenase, enhanced oxygen supply and consumption, alleviated myocardial interstitial edema and less myocardial fiber breakage, which greatly improved the survival rate of animals (P < 0.05). Conclusion Sterofundin obviously improves the heart function and thus plays a protective role in organ functions in septic rats.

Objective To observe the early therapeutic effects of a mitochondrial fission inhibitor, mitochondrial division inhibitor 1 (Mdivi-1), on the traumatic shock rats at high altitude. Methods SD rats were rapidly transported (airlift) from the plain (Chongqing) to the plateau (Lhasa, 3 600 m altitude). After 72 h, the traumatic shock model of rats at high altitude was prepared by free bleeding from splenic artery disconnection until mean arterial pressure (MAP) fell to 40 mmHg. The animals were divided into 5 groups: sham-operation group, shock group, Lactate Ringer's (LR) solution control group, and LR combined with 0.1 and 0.5 mg/kg Mdivi-1 groups. Then the experiments were designed as 2 parts. The rats in the first part were resuscitated with mere LR solution or combined with 0.1 or 0.5 mg/kg Mdivi-1 without hemostatic treatment. With the MAP maintained at 50-60 mmHg, the changes of MAP, bleeding volume, fluid infusion volume and survival rate were observed in each group. In the second part, bleeding control was performed by ligation of the spleen artery after 1 h of low-pressure resuscitation, and definitive resuscitation was continuously given. The changes of blood loss, infusion volume, organ functions, tissue oxygen partial pressure, lung and brain water content and animal survival were subsequently investigated. Results When LR solution was used for low-pressure resuscitation without hemostatic treatment, the MAP of rats was maintained at 50-60 mmHg for about 1 h, and then began to drop gradually rather than rise after increasing the amount of fluid input, with the bleeding volume soared obviously. Whereas Mdivi-1 combination treatment maintained MAP at 50-60 mmHg for about 3 h, and significantly reduced the bleeding volume and fluid infusion. Further studies showed that in the hemostatic resuscitation treatment, the rats of the LR control group still had a rather low level of tissue oxygen partial pressure, with elevated water contents in the lung and brain, and seriously impaired functions of vital organs such as the heart, liver and kidney. However, Mdivi-1 (0.1 or 0.5 mg/kg) treatment remarkably improved the damage, increased the tissue oxygen partial pressure, reduced the water contents in the lung and brain, alleviated the impairment of the heart, liver and kidney, and greatly prolonged the survival time of shock animals. Conclusion Mdivi-1 is suitable for the early treatment of traumatic shock at high altitude, which can improve organ functions and extend the golden time of treatment.

目的 观察精氨酸血管加压素(AVP)对海水浸泡合并非控制性失血休克大鼠的复苏效果.方法 采用15℃低温海水联合脾切除的非控制性失血休克Sprague-Dawley(SD)雄性大鼠72只,14～16周龄,体重(230±20)g,按随机数字表法将大鼠分为单纯乳酸林格液(LR)复苏对照组(LR组),去甲肾上腺素(NE)联合LR复苏组(NE组)、AVP联合LR复苏组(AVP组),各24只.休克后各实验组大鼠分别静脉输注LR、NE(5μg/kg)+LR以及AVP(0.1U/kg)+LR.观察AVP对休克大鼠失血率、复苏液体量、凝血功能、酸中毒及存活的影响.结果 经海水浸泡合并非控制性失血休克后,在彻底止血前低压复苏阶段AVP组失血率(49±3.6)％较LR组大鼠失血率(52±6.0)％减少,NE组失血率较LR组增加.确定性治疗阶段AVP组复苏液体量(32.9±2.23)mL较LR组复苏液体量(66.7±5.63)mL显著降低(P<0.01),NE组复苏液体量(47.0±3.50)mL减少,但与LR组比较无显著差异(P>0.05).复苏结束后,AVP组凝血功能显著改善,表现为凝血酶原时间国际化比值(PT-INR)、凝血酶原时间(PT)较LR组显著缩短(P<0.05,P<0.01),分别为(2.0±0.11)s和(23.2±1.20)s;NE组凝血功能改善不显著(P>0.05).血气分析提示各组大鼠pH值均恢复至7.3左右,AVP组氧分压(PaO2)较LR组和NE组有一定程度增加,至(153.0±14.49)mmHg.AVP组平均存活时间显著延长至26h,24h存活率为50％;NE组和LR组平均存活时间分别为20h和16h,24h存活率均仅为25％.结论 AVP能显著减少海水浸泡合并非控制性失血休克大鼠的失血率和输液量,改善凝血功能和血气,延长存活时间,提高存活率.

目的:探讨钙敏感性受体(CaSR)抑制剂Calhex231(Cal)是否通过甲状旁腺素(PTH)-肾上腺素受体(AR)途径参与创伤失血性休克大鼠血管低反应性的调节.方法:检测Cal对创伤失血性休克大鼠血PTH水平的影响,并观察外源给予PTH对正常和休克大鼠血压的影响;Western blot法检测Cal对大鼠肠系膜上动脉(SMA)以及外源给予PTH对大鼠原代血管平滑肌细胞(VSMC)中2种AR亚型(α1-AR和β1-AR)蛋白表达水平的影响.结果:创伤失血性休克后大鼠血PTH水平显著升高,Cal治疗能够显著降低血PTH水平(P<0.01).外源给予PTH能显著降低正常大鼠血压.在组织水平上,Cal能提高创伤失血性休克大鼠SMA中α1-AR蛋白表达水平(P<0.05);在细胞水平上,外源给予PTH能使大鼠原代VSMC中α1-AR蛋白表达水平降低,Cal能拮抗PTH降低α1-AR蛋白表达的作用(P<0.05).结论:CaSR抑制剂Cal可通过降低血PTH水平、上调血管α1-AR蛋白表达水平而发挥改善休克后血管低反应性的作用.

Background: Sepsis/septic shock is a common complication in the intensive care unit, and the opening of the mitochondrial permeability transition pore (mPTP), as well as the endoplasmic reticulum stress (ERS), play important roles in this situation. Whether the combination of anti-ERS and anti-mPTP by 4-phenylbutyric acid (PBA) and Cyclosporine A (CsA) could benefit sepsis is unclear. Methods: The cecal ligation and puncture-induced septic shock models were replicated in rats, and lipopolysaccharide (LPS)-challenged primary vascular smooth muscle cells and H9C2 cardiomyocytes in vitro models were also used. The therapeutic effects of CsA, PBA, and combined administration on oxygen delivery, cardiac and vascular function, vital organ injury, and the underlying mechanisms were observed. Results: Septic shock significantly induced cardiovascular dysfunction, hypoperfusion, and organ injury and resulted in high mortality in rats. Conventional treatment including fluid resuscitation, vasoactive agents, and antibiotics slightly restored tissue perfusion and organ function in septic rats. Supplementation of CsA or PBA improved the tissue perfusion, organ function, and survival of septic shock rats. The combined application of PBA and CsA could significantly enhance the beneficial effects, compared with using PBA or CsA alone. Further study showed that PBA enhanced CsA-induced cardiovascular protection, which contributed to better therapeutic effects. Conclusion: Anti-ERS and anti-mPTP-opening by the combination of PBA and CsA was beneficial to septic shock. PBA enforced the CsA-associated cardiovascular protection and contributed to the synergetic effect.

在建立传统公共卫生间和经过改造后的卫生间模型的基础上,分别对卫生间内污染物的浓度场和速度场分布进行数值模拟,并对模拟结果进行比较和分析.传统卫生间内气流组织分布杂乱无章,经改造后的卫生间,气流组织形态基本呈单向矢流,气流直接从呼吸区到污染区再排放到室外,污染物浓度分布基本在排风口处较低区域.改变卫生间内进、排风口相对位置以及进风口形式,采用百叶风口,使卫生间内气流整体呈单向矢流,污染物扩散影响范围较其他情况明显减小.

ABSTRACT:Aquaporins (AQPs) are a group of membrane proteins related to water permeability. Studies have shown that AQPs play a vital role in various diseases. Whether AQPs participate in regulating vascular permeability after sepsis and whether the subtype of AQPs is related are unknown. Ss-31, as a new antioxidant, had protective effects on a variety of diseases. However, whether Ss-31 has a protective effect on pulmonary vascular permeability in sepsis and whether its effect is related to AQPs are unclear. Using the cecum ligation perforation-induced septic rat and LPS-treated pulmonary vein endothelial cells, the role of AQPs in the regulation of the permeability of pulmonary vascular and its relationship to Ss-31 were studied. The results showed that the pulmonary vascular permeability significantly increased after sepsis, meanwhile the expressions of AQP3, 4, and 12 increased. Among those, the AQP3 was closely correlated with pulmonary vascular permeability. The inhibition of AQP3 antagonized the increase of the permeability of monolayer pulmonary vein endothelial cells. Further study showed that the expression of caveolin-1 (Cav-1) increased and occludin decreased after sepsis. The inhibition of AQP3 antagonized the decrease of Cav-1 and the increase of occludin in sepsis. Antioxidant Ss-31 decreased the expression of AQP3 and ROS levels. At the same time, Ss-31 improved pulmonary vascular permeability and prolonged survival of sepsis rats. In conclusion, AQP3 participates in the regulation of pulmonary vascular permeability after sepsis, and the antioxidant Ss-31 has a protective effect on pulmonary vascular permeability by downregulating the expression of AQP3 and inhibiting ROS production.