To evaluate the process from systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS) and probe the therapeutic strategies for elderly patients, we retrospectively studied the clinical data of SIRS and MODS in 292 elderly patients with surgical abdominal emergency. Results: On admission, the morbidity rate of SIRS was 41.1%. Afterwards the morbidity rate of MODS was 14.2%, and the mortality rate of the elderly patients with SIRS was 11.7%. After 48 hours of therapy, MODS was developed in 40.5% of the cases also with SIRS. Of all the 292 elderly patients, 19 cases (6.5%) developed MODS and 16 patients (84.2%) died. Conclusion: The outcome of the patients with surgical abdominal emergency may be improved if SIRS is early diagnosed, the cause of SIRS after 48 hours therapy is well defined and the body inflammatory response is properly regulated.
ObjectiveTo investigate the protective effect and mechanism of arbutin on LPS induced Acute lung injury in mice. Methods SPF BCLB/C mice were randomly divided into control group, model group,arbutin group, and arbutin+PI3K inhibitor group.arbutin group and arbutin+PI3K group were intervened with corresponding drugs respectively; Constructing an ALI model by intranasal instillation of LPS into mice; After modeling for 6 hours, the mice were killed. After staining the lung tissue slices, observe the pathological changes of the lung tissue and evaluate the lung injury score, and calculate the wet to dry weight ratio (W/D); ELISA method was used to determine the levels of TNF-a and IL-6 in serum and bronchoalveolar lavage fluid (BALF); Measure the ROS content, MDA level,and MPO activity in the lungs; Western blot method was used to detect the expression of PI3K/Akt/mTOR pathway related proteins and autophagy related proteins Beclin-1 and LC3II/I. ResultsCompared with the control group, the pathological changes in the lung tissue of model group mice worsened, and the W/D and lung injury scores increased, The levels of IL-6 and TNF-a in BALF and serum was increased, The ROS content, MDA expression and MPO activity in the lungs was increased,the expression of Beclin-1 and LC3II/I in the lungs was increased. The expression of PI3K/Akt/mTOR pathway related proteins in the lungs decreased (P<0.05). Compared with the model group, the pathological changes in the lung tissue of arbutin group mice were alleviated, with a decrease in W/D and lung injury score, The levels of IL-6 and TNF-a in BALF and serum decrease,ROS content, MDA expression and MPO activity in lung were decreased.The expression of PI3K/Akt/mTOR pathway related proteins in the lung was increased, The expression of Beclin-1 and LC3II/I decreased. However, the appeal performance was partially blocked in the arbutin+PI3K group after the administration of LY294002.ConclusionsArbutin regulates autophagy through PI3K/Akt/mTOR pathway to inhibit inflammatory response and oxidative stress in LPS-induced ALI mice, and plays a protective role in LPS-induced ALI.
Abstract: Objective To investigate the effect of liposomal prostaglandin E1 (LipoPGE1) on inflammatory reaction during cardiopulmonary bypass (CPB) coronary artery bypass grafting (CABG). Methods Between July 2006 and December 2008, a total of 32 patients undergoing CABG were randomly divided into two groups of 16 patients each using a random digits table. The experimental group had 9 male and 7female patients with a mean age of 54.4±18.1 years; each patient received 15.0ng/(kg·min) of LipoPGE1 by venous pump through the central vein throughouttheCPB procedure. The control group had 9 male and 7 female patients with a mean age of 54.8±20.4 years, who were treated identically to the experimental group except did not receive LipoPGE1. Arterial blood samples were taken before CPBand at the 1st, 2nd, 6th, and 24th hour after open aorta ascendens. The levels of interleukin6(IL6), tumor necrosis factorα (TNFα), and soluble intercellular adhesion molecule1 (sICAM1) were tested and compared. Results In both groups, levels of IL6, TNFα, and sICAM1 were all gradually increased after the ascending aorta was opened, and they reached their highest levels at the 6th hour after open aorta ascendens. In the experimental group, at every time point afterthe ascending aorta was open, levels of IL6 (24th hour after open aorta ascendens: 16.1±2.2 μg/L vs. 19.2±4.5 μg/L,Plt;0.05), TNFα (24th hour after open aorta ascendens: 1.8±04 μg/L vs. 2.2±0.5 μg/L,Plt;0.05), and sICAM1 (24th hour after open aorta ascendens: 233.6±36.6 μg/L vs. 294.2±55.7 μg/L,Plt;0.05) were significantly lower than those of the control group. 〖WTHZ〗Conclusion LipoPGE1 effectively reduces the aggregation of polymorphonuclear neutrophilic leukocytes, inhibits activation of vascular endothelialcells, and decreases systemic inflammatorome during CPB.
ObjectiveTo investigate the effects of esophageal cooling (EC) on lung injury and systemic inflammatory response after cardiopulmonary resuscitation in swine.MethodsThirty-two domestic male white pigs were randomly divided into sham group (S group, n=5), normothermia group (NT group, n=9), surface cooling group (SC group, n=9), and EC group (n=9). The animals in the S group only experienced the animal preparation. The animal model was established by 8 min of ventricular fibrillation and then 5 min of cardiopulmonary resuscitation in the other three groups. A normal temperature of (38.0±0.5)℃ was maintained by surface blanket throughout the experiment in the S and NT groups. At 5 min after resuscitation, therapeutic hypothermia was implemented via surface blanket or EC catheter to reach a target temperature of 33℃, and then maintained until 24 h post resuscitation, and followed by a rewarming rate of 1℃/h for 5 h in the SC and EC groups. At 1, 6, 12, 24 and 30 h after resuscitation, the values of extra-vascular lung water index (ELWI) and pulmonary vascular permeability index (PVPI) were measured, and meanwhile arterial blood samples were collected to measure the values of oxygenation index (OI) and venous blood samples were collected to measure the serum levels of tumor necrosis factor-α (TNF-α) and inerleukin-6 (IL-6). At 30 h after resuscitation, the animals were euthanized, and then the lung tissue contents of TNF-α, IL-6 and malondialdehyde, and the activities of superoxide dismutase (SOD) were detected.ResultsAfter resuscitation, the induction of hypothermia was significantly faster in the EC group than that in the SC group (2.8 vs. 1.5℃/h, P<0.05), and then its maintenance and rewarming were equally achieved in the two groups. The values of ELWI and PVPI significantly decreased and the values of OI significantly increased from 6 h after resuscitation in the EC group and from 12 h after resuscitation in the SC group compared with the NT group (all P<0.05). Additionally, the values of ELWI and PVPI were significantly lower and the values of OI were significantly higher from 12 h after resuscitation in the EC group than those in the SC group [ELWI: (13.4±3.1) vs. (16.8±2.7) mL/kg at 12 h, (12.4±3.0) vs. (16.0±3.6) mL/kg at 24 h, (11.1±2.4) vs. (13.9±1.9) mL/kg at 30 h; PVPI: 3.7±0.9 vs. 5.0±1.1 at 12 h, 3.4±0.8 vs. 4.6±1.0 at 24 h, 3.1±0.7 vs. 4.2±0.7 at 30 h; OI: (470±41) vs. (417±42) mm Hg (1 mm Hg=0.133 kPa) at 12 h, (462±39) vs. (407±36) mm Hg at 24 h, (438±60) vs. (380±33) mm Hg at 30 h; all P<0.05]. The serum levels of TNF-α and IL-6 significantly decreased from 6 h after resuscitation in the SC and EC groups compared with the NT group (all P<0.05). Additionally, the serum levels of IL-6 from 6 h after resuscitation and the serum levels of TNF-α from 12 h after resuscitation were significantly lower in the EC group than those in the SC group [IL-6: (299±23) vs. (329±30) pg/mL at 6 h, (336±35) vs. (375±30) pg/mL at 12 h, (297±29) vs. (339±36) pg/mL at 24 h, (255±20) vs. (297±33) pg/mL at 30 h; TNF-α: (519±46) vs. (572±49) pg/mL at 12 h, (477±77) vs. (570±64) pg/mL at 24 h, (436±49) vs. (509±51) pg/mL at 30 h; all P<0.05]. The contents of TNF-α, IL-6, and malondialdehyde significantly decreased and the activities of SOD significantly increased in the SC and EC groups compared with the NT group (all P<0.05). Additionally, lung inflammation and oxidative stress were further significantly alleviated in the EC group compared with the SC group [TNF-α: (557±155) vs. (782±154) pg/mg prot; IL-6: (616±134) vs. (868±143) pg/mg prot; malondialdehyde: (4.95±1.53) vs. (7.53±1.77) nmol/mg prot; SOD: (3.18±0.74) vs. (2.14±1.00) U/mg prot; all P<0.05].ConclusionTherapeutic hypothermia could be rapidly induced by EC after resuscitation, and further significantly alleviated post-resuscitation lung injury and systemic inflammatory response compared with conventional surface cooling.
ObjectiveTo investigate the feasibility and safety of non-intubation anesthesia in thoracic surgery.MethodsFrom September 2017 to December 2019, 296 patients were operated at department of thoracic surgery in our hospital. There were 167 males and 129 females with an average age of 50.69±12.95 years, ranging from 16 to 76 years. The patients were divided into two groups according to whether they were intubated: 150 patients were in a non-intubation group, including 83 males and 67 females with an average age of 49.91±13.59 years, ranging from 16 to 76 years, and 146 patients were in an intubation group including 84 males and 62 females with an average age of 51.49±12.26 years, ranging from 16 to 74 years. Intraoperative data, postoperative recovery, inflammatory response of the two groups were compared.ResultsThere was no statistical difference between the two groups in operation time, blood loss, the lowest oxygen saturation or other indicators (P>0.05). But the highest partial pressure of carbon dioxide of the non-intubation group was higher than that of the intubation group (P=0.012). The non-intubation group was superior to the intubation group in postoperative recovery and inflammatory response (P<0.05).ConclusionThe non-intubation anesthesia is safe and maneuverable in thoracic surgery, and it has some advantages in accelerating postoperative rehabilitation.
Although great progress has been achieved in the techniques and materials of cardiopulmonary bypass (CPB), cardiac surgery under CPB is still one of the surgeries with the highest complication rate. The systemic inflammatory response is an important cause of complications, mainly characterized by activation of innate immune cells and platelets, and up-regulation of inflammatory cytokines. After activation, a variety of molecules on the membrane surface are up-regulated or down-regulated, which can amplify tissue inflammatory damage by releasing cytoplasmic protease and reactive oxygen species, and activate multiple inflammatory signaling pathways in the cell, ultimately leading to organ dysfunction. Therefore, the expression of these cell membrane activation markers is not only a marker of cell activation, but also plays an important role in the process of vital organ injury after surgery. Identification of these specific activation markers is of great significance to elucidate the mechanisms related to organ injury and to find new prevention and treatment methods. This article will review the relationship between these activated biomarkers in the innate immune cells and vital organ injuries under CPB.
Abstract: Objective To investigate the effect of modified ultrafiltration on attenuating the inflammatory reaction and endothelial cell activation or damage after cardiopulmonary bypass (CPB). Methods Forty patients undergoing cardiac operation with CPB were randomly divided into two groups. Ult rafiltration group ( n = 20) : patients underwent modified ultrafiltration after CPB; control group ( n = 20 ) : without ultrafiltration. Plasma concentrations of soluble intercellular adhesion molecules-1 ( s ICAM -1) and tumor necrosis factor-α (TNF-α) were determined with enzyme linked immunosorbent assay and radioimmunity pre-operat ively (baseline) , at the end of CPB, 4h and 24h post-operatively in both groups. Results The concentrations of sICAM -1 in the cont rol group at 4h and 24h po st-operatively were higher than those pre-operatively (P lt; 0. 01). The concentrations sICAM -1 in the ultrafiltrat ion group in pre-operatively and at the end of CPB were not significantly different from that of the control group, but they were lower at 4h and 24h post-operatively (269. 6±33. 8Lg/L vs. 409. 6±37. 3Lg/L , 245. 9±32. 2Lg/L vs. 379. 3±35. 7Lg/L ; P lt; 0. 01). In the ultrafiltration group, the concentration of TN F-α at the end of CPB and 4h post-operatively were higher than that pre-operatively (P lt; 0. 01). The concent rations of TNF-α in the ultrafiltration group at 24h post-operatively recoved to the pre-operative level (0. 177±0. 024Lg/L vs. 0. 172±0. 030Lg/L ; P gt;0.05). In the control group, the concentration of TN F-α was higher at the end of CPB than that pre-operatively (P lt;0.01) , and decreased slightly at 4h and 24h post-operatively, but remained higher than those pre-operat ively (0. 264±0.045Lg/L vs. 0.174±0.033Lg/L , 0.218±0.028Lg/L vs. 0.174±0. 033Lg/L ; P lt; 0. 05). Conclus ion CPB is known to induce inflammatory reaction and endothelial cell activation or damage. Modified ultrafiltration appears to attenuate these adverse reactions and is beneficial to postoperative convalescence.
目的探讨血清胆红素升高在急性阑尾炎坏疽、穿孔中的诊断价值。 方法回顾性分析2011年6月至2013年8月期间我院住院行手术治疗的急性阑尾炎患者的临床病理资料，比较多种指标诊断急性复杂阑尾炎的准确性。 结果复杂阑尾炎患者血清总胆红素（STB）水平明显高于非复杂阑尾炎患者（P＜0.001）。STB升高诊断复杂阑尾炎的敏感性及特异性分别为33.3%和86.2%，而血清直接胆红素(SDB）升高（≥6.65μmol/L）诊断复杂阑尾炎的敏感性及特异性分别为78.1%和63.5%。系统炎症反应（SIRS）评分与STB联合诊断具最佳诊断效能，受试者操作特征曲线下面积为0.741，而血清白细胞计数（特异性40.7%）诊断准确性相对较低。 结论SDB升高诊断急性阑尾炎坏疽、穿孔的准确性较佳，STB与SIRS评分联合诊断可作为早期鉴别诊断复杂阑尾炎的参考指标。
Objective To investigate the feasibility of selenium-methylselenocysteine (SMC) to promote peripheral nerve regeneration and its mechanism of action. Methods Rat Schwann cells RSC96 cells were randomly divided into 5 groups, which were group A (without any treatment, control group), group B (adding 100 μmol/L H2O2), group C (adding 100 μmol/L H2O2+100 μmol/L SMC), group D (adding 100 μmol/L H2O2+200 μmol/L SMC), group E (adding 100 μmol/L H2O2+400 μmol/L SMC); the effect of SMC on cell proliferation was detected by MTT method, and the level of oxidative stress was detected by immunofluorescence for free radicals [reactive oxygen species (ROS)] after determining the appropriate dose group. Thirty-six 4-week-old male Sprague Dawley rats were randomly divided into 3 groups, namely, the sham operation group (Sham group), the sciatic nerve injury group (PNI group), and the SMC treatment group (SMC group), with 12 rats in each group; the rats in the PNI group were fed with food and water normally after modelling operation, and the rats in the SMC group were added 0.75 mg/kg SMC to the drinking water every day. At 4 weeks after operation, the sciatic nerves of rats in each group were sampled for neuroelectrophysiological detection of highest potential of compound muscle action potential (CMAP). The levels of inflammatory factors [interleukin 17 (IL-17), IL-6, IL-10 and oxidative stress factors catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA)] were detected by ELISA assay. The luxol fast blue (LFB) staining was used to observe the myelin density, fluorescence intensity of glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) was observed by immunofluorescence staining, and myelin morphology was observed by transmission electron microscopy with measurement of axon diameter. Western blot was used to detect the protein expressions of p38 mitogen-activated protein kinases (p38MAPK), phosphorylated p38MAPK (p-p38MAPK), heme oxygenase 1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). ResultsMTT assay showed that the addition of SMC significantly promoted the proliferation of RSC96 cells, and the low concentration could achieve an effective effect, so the treatment method of group C was selected for the subsequent experiments; ROS immunofluorescence test showed that group B showed a significant increase in the intensity of ROS fluorescence compared with that of group A, and group C showed a significant decrease in the intensity of ROS fluorescence compared with that of group B (P<0.05). Neuroelectrophysiological tests showed that the highest potential of CMAP in SMC group was significantly higher than that in PNI and Sham groups (P<0.05). ELISA assay showed that the levels of IL-6, IL-17, and MDA in PNI group were significantly higher than those in Sham group, and the levels of IL-10, SOD, and CAT were significantly lower; the levels of IL-6, IL-17, and MDA in SMC group were significantly lower than those in PNI group, and the levels of IL-10, SOD, and CAT were significantly higher (P<0.05). LFB staining and transmission electron microscopy showed that the myelin density and the diameter of axons in the SMC group were significantly higher than those of the PNI group and the Sham group (P<0.05). Immunofluorescence staining showed that the fluorescence intensity of GFAP and MBP in the SMC group were significantly stronger than those in the PNI group and Sham group (P<0.05). Western blot showed that the relative expressions of Nrf2 and HO-1 proteins in the SMC group were significantly higher than those in the PNI group and Sham group, and the ratio of p-p38MAPK/p38MAPK proteins was significantly higher in the PNI group than that in the SMC group and Sham group (P<0.05). Conclusion SMC may inhibit oxidative stress and inflammation after nerve injury by up-regulating the Nrf2/HO-1 pathway, and then inhibit the phosphorylation of p38MAPK pathway to promote the proliferation of Schwann cells, which ultimately promotes the formation of myelin sheaths and accelerates the regeneration of peripheral nerves.
ObjectiveTo summarize the mechanism of neutrophil extracellular traps (NETs) in hepatic ischemia-reperfusion injury (HIRI) and the research progress in targeting NETs to reduce HIRI, providing valuable reference for reducing HIRI. MethodThe related literatures at home and abroad about the role of NETs in the pathogenesis of HIRI and target NETs to alleviate HIRI were retrieved and reviewed. ResultsHIRI usually appeared in the process of liver surgery and was a common clinical problem, which occured in situations such as liver surgery, organ transplantation, liver ischemia and so on. This kind of injury would lead to tissue necrosis, inflammatory response and oxidative stress, which was a major cause of hepatic dysfunction and multiple organ failure after hepatic surgery, greatly increases the complications and mortality after hepatic surgery. NETs played a crucial role in the aseptic inflammatory response induced by hepatic ischemia/reperfusion. During hepatic ischemia-reperfusion, neutrophils promoted inflammatory cascade reactions and cytokine storms by forming NETs, exacerbating damage caused by hepatic ischemia-reperfusion. At present, some experimental and clinical studies had shown that inhibiting the formation of NETs or eliminating the formed NETs could alleviate the hepatic ischemia-reperfusion injury and improve the prognosis. ConclusionsTargeting NETs may become a new method for treating hepatic ischemia-reperfusion injury. In the future, it is foreseeable that more experiments and clinical trials will be conducted on targeted NETs for the treatment of hepatic ischemia-reperfusion injury. And gradually establish more comprehensive and effective treatment strategies, thereby providing new ways to improve the prognosis of hepatic surgery patients in clinical practice.