The stress response can be triggered during the perioperative period by tension, fear, anesthesia, surgical trauma, and various postoperative adverse stimuli, leading to significant changes in the endocrine, metabolic, and immune systems of patients. In particular, immunosuppression induced by the stress response has adverse effects on the postoperative recovery of patients. As acupuncture stimulation-related technologies have been rapidly developed and applied in recent years, a number of basic and clinical studies have confirmed that acupoint stimulation can regulate the immune system via local, neurological, and endocrine pathways. Moreover, acupoint stimulation treatment has also been shown to reduce the adverse effects of immunosuppression by affecting the release of various cytokines, such as interleukin (IL) 1, IL-2, IL-4, IL-6, IL-10, IFN-γ, and tumor necrosis factor (TNF) β, immunoglobulins, complement proteins, and T cell markers such as CD3, CD4, and CD4/CD8 via the regulation of macrophages, neutrophils, NK cells, and endogenous opioids. In addition, acupuncture stimulation treatment during the perioperative period can also significantly decrease the amount of anesthetic required for anesthesia, effectively reduce nausea and vomiting, relieve post-operative pain, and accelerate the recovery of physiological functions. Therefore, acupuncture stimulation treatment has shown important potential for clinical applications.

This study was designed to investigate the neuroprotective effect of hyperoxygenate hydrogen-rich saline (HOHS) against brain injury induced by carbon monoxide (CO) poisoning in rats. A rat model of CO poisoning was established by administering CO via intraperitoneal injection to male Sprague-Dawley rats. Forty-eight adult male rats were randomly divided into the following groups: normal control group (NG), CO poisoning group (CO), HOS treatment group (hyperoxygenated solution, HOS) and HOHS treatment group (HOHS). After CO poisoning, the carboxyhemoglobin (COHb) contents in the blood of rats in all the CO poisoning groups were increased significantly. However, HOS and HOHS significantly decreased COHb contents, furthermore, the HOHS group had lower COHb contents than the HOS group. Arterial oxygen partial pressure (PaO2) and arterial oxygen saturation (SaO2) results showed that HOS and HOHS could improve the oxygenation of the rats with CO poisoning. Compared with the CO group, the HOS group and the HOHS group had persistently neuroprotective effect on CO-induced brain injury, as assessed by modified neurological severity score (mNSS), furthermore, the HOHS group had better neurological functional recovery than the HOS group. The neuronal apoptosis induced by CO was also evaluated. Except the NG group, all the CO-poisoning groups had varying degrees of neuronal apoptosis. There was lesser degree of neuronal apoptosis in both the HOS group and the HOHS group than that in the CO group. Moreover, the HOHS group had more minor degree of neuronal apoptosis than the HOS group. Compared with the CO group, the free radicals production in the HOS group and the HOHS group were significantly inhibited. In addition, there were significantly difference in the free radicals production between the HOS group and the HOHS group. We could conclude that HOHS exerted a stronger neuroprotective effect against CO-induced brain injury than HOS, and the neuroprotective mechanism of HOHS may be related with inhibition of both neuronal apoptosis and free radicals.

Background: Hemorrhagic shock could induce acute lung injury (ALI), which is associated with cell hypoxia, lung tissue inflammation, free radical damage, and excessive cell apoptosis. Our previous studies demonstrated that hyperoxygenated solution could alleviate cell hypoxia. Furthermore, hydrogen-rich solution (HS) could relieve lung tissue inflammation, free radical damage and excessive cell apoptosis. Therefore we hypothesize that Hyperoxygenated Hydrogen-rich solution (HOHS) can protect the lung against ALI. Materials and methods: SD rats were randomly divided into five groups (n = 6 at each time point in each group) and were exposed to Hemorrhagic shock induced ALI, and then treated with lactated Ringer's solution (LRS), hyperoxygenated solution, HS, and HOHS, respectively. The protective effects of these solutions were assessed using methods as follows: arterial blood samples were collected for blood gas analysis; Bronchoalveolar lavage fluid was collected for cell count and protein quantification; lung tissue samples were collected to measure wet/dry ratio, as well as levels of T-SOD, MDA, TNF-alpha, and IL-6; Caspase-3 and TUNEL-positive cells, and pathological changes were observed under light microscope; ALI was scored using the Smith scoring method; ultrastructural changes of lung tissues were further observed with transmission electron microscopy. Results: The results indicated that PaO2, PaCO2, and T-SOD increased in the three treatment groups (P < 0.05), most significantly in the HOHS group (P < 0.01) compared with the LRS group; and conversely that the levels of lactate, MDA, TNF-alpha and IL-6, cell count, protein content, caspase-3 and TUNEL-positive cells as well as ALI score decreased in the three treatment groups (P < 0.05), most significantly in the HOHS group (P < 0.01) compared with the LRS group. Morphological observation with optical microscope and electron microscopy showed that compared with the LRS group, cell damage in the three treatment groups improved to a varying extent, especially evident in the HOHS group. Conclusions: These findings demonstrate that HOHS can protect the lung against ALI induced by hemorrhagic shock. (C) 2019 Elsevier Inc. All rights reserved.

In recent years,the rapid development of medical and pharmaceutical preparation processes has greatly pro -moted the development of local anesthetic(LA).The rapid development of microsphere,liposomes,emulsifier,hydrogel tech-nology has extended the acting time and improved the effect of LA.However,with the research and development and applica-tion of new formulations of LA,the adverse reactions of LA like allergies,peripheral and central nervous system toxicity, have attracted the attention of the medical community.It is important to further understand the development, preparation, anesthesia characteristics,adverse reaction and prevention measures of these new forms of LA,which can also provide refer-ence for the clinical application of LA,and reduce the occurrence of adverse reactions,and better serve the patients.

Previous studies have proven that paired immunoglobulin-like receptor B (PirB) plays a crucial suppressant role in neurite outgrowth and neuronal plasticity after central nervous system injury. However, the role of PirB in neuronal survival after cerebral ischemic injury and its mechanisms remains unclear. In the present study, the role of PirB is investigated in the survival and apoptosis of cerebral cortical neurons in cultured primary after oxygen and glucose deprivation (OGD)-induced injury. The results have shown that rebarbative PirB exacerbates early neuron apoptosis and survival. PirB gene silencing remarkably decreases early apoptosis and promotes neuronal survival after OGD. The expression of bcl-2 markedly increased and the expression of bax significantly decreased in PirB RNAi-treated neurons, as compared with the control- and control RNAi-treated ones. Further, phosphorylated TrkB and mTOR levels are significantly downregulated in the damaged neurons. However, the PirB silencing markedly upregulates phosphorylated TrkB and mTOR levels in the neurons after the OGD. Taken together, the overexpression of PirB inhibits the neuronal survival through increased neuron apoptosis. Importantly, the inhibition of the phosphorylation of TrkB and mTOR may be one of its mechanisms.

Background: It is not known whether simultaneous delivery of hydrogen and oxygen can reduce injury caused by hemorrhagic shock and resuscitation (HSR). This study investigated the therapeutic potential of hyperoxygenated hydrogenerich solution (HHOS), a combined hydrogen/oxygen carrier, in a rat model of HSR-induced liver injury. Materials and methods: Rats (n = 60) were randomly divided into 5 groups (n = 6 per group at each time point). One group underwent sham operation, and the others were subjected to severe hemorrhagic shock and then treated with lactated Ringer's solution (LRS), hydrogen-rich solution, hyperoxygenated solution, or HHOS. At 2 and 6 h after resuscitation, blood samples (n = 6) were collected from the femoral artery and serum concentrations of alanine aminotransferase and aspartate aminotransferase (AST) were measured. Rats were then sacrificed, and histopathological changes in the liver were evaluated by quantifying the percentage of apoptotic cells by caspase-3 immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick-end labeling. Inflammation was assessed by assessing malondialdehyde content and tumor necrosis factor-a, and interleukin (IL)-6 expression. Results: Compared to lactated Ringer's solution, hydrogen-rich solution, or hyperoxygenated solution groups, serum AST and alanine aminotransferase levels and IL-6, tumor necrosis factor-a, and malondialdehyde expression in liver tissue were decreased by HHOS treatment. The number of caspase-3-and terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells was decreased (P < 0.05) by HHOS treatment, 2 and 6 h after resuscitation. Conclusions: HHOS has protective effects against liver injury in a rat model of HSR. (C) 2017 Elsevier Inc. All rights reserved.

Objective To evaluate the effect of hyperoxygenated solution on myocardial injury in the rats with acute carbon monoxide (CO) poisoning.Methods Thirty pathogen-free adult male SpragueDawley rats,weighing 250-300 g,were randomly divided into 5 groups (n=6 each) using a random number table:control group (C group),acute CO poisoning group (ACP group),and different doses of hyperoxygenated solution groups (HP1-3 groups).CO 120 ml/kg was injected intraperitoneally to establish the model of acute CO poisoning.Hyperoxygenated solution 10,15 and 20 ml/kg were infused via the caudal vein at 1 h after intraperitoneal injection of CO in HP1-3 groups,respectively.At 24 h after intraperitoneal injection of CO,blood samples were collected from the caudal vein for determination of plasma creatine kinase (CK),creatine kinase-MB (CK-MB),lactic dehydrogenase (LDH) and alpha-hydroxybutyrate acid dehydrogenase (α-HBDH) activities using the automatic biochemical analyzer.The rats were then sacrificed,and myocardial specimens were obtained for examination of the pathological changes with a light microscope.Results Compared with group C,the plasma LDH,α-HBDH,CK and CK-MB activities were significantly increased in ACP and HP1-3 groups (P＜0.01).Compared with group ACP,the plasma LDH,α-HBDH,CK and CK-MB activities were significantly decreased in HP1-3 groups (P＜0.05 or 0.01).Compared with group HP1,the plasma LDH,α-HBDH,CK and CK-MB activities were significantly decreased in HP2,3 groups (P＜0.05).The pathological changes of myocardium were significantly attenuated in HP1-3 groups as compared with group ACP.Conclusion Hyperoxygenated solution can attenuate myocardial injury in the rats with acute CO poisoning.

Objective To evaluate the effects of hydrogen-rich saline on liver injury in a rat model of hemorrhagic shock and resuscitation.Methods Forty-eight pathogen-free male Sprague-Dawley rats,aged 6-8 weeks,weighing 150-250 g,were randomly divided into 3 groups (n =16 each) using a random number table:sham operation group (group Sham),hemorrhagic shock and resuscitation group (group HR),and hydrogen-rich saline group (group HRS).Severe hemorrhagic shock was induced according to the method described by Wiggers.Lactated Ringer's solution and hydrogen-rich saline were given for resuscitation in HR and HRS groups,respectively.At 6 h after resuscitation,blood samples were collected from the femoral artery for determination of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations by automatic biochemical analyzer.The rats were then sacrificed,and liver specimens were obtained for examination of histopathological changes (using light microscope) and for determination of total superoxide dismutase (T-SOD) activity,malondialdehyde (MDA) content,and tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) concentrations (using the corresponding kits).Results Compared with group Sham,the levels of ALT and AST in serum and IL-6,TNF-α,T-SOD and MDA in liver tissues were significantly increased in HR and HRS groups (P＜0.01).Compared with group HR,the levels of ALT and AST in serum and IL-6,TNF-α,and MDA in liver tissues were significantly decreased,and the T-SOD level was significantly increased in group HRS (P＜0.01).The histopathological changes of livers were significantly attenuated in group HRS as compared with group HR.Conclusion Hydrogen-rich saline can reduce liver injury in a rat model of hemorrhagic shock and resuscitation.

目的:旨在证实电针预处理百会穴对脑缺血损伤的保护作用及HIF-1α的相关机制.方法:将雄性SD大鼠80只随机分为5组(n=16):假手术组(Sham),对照组(CON),电针预处理组(EA),HIF-1α抑制剂组(2ME2)和电针预处理+HIF-1α抑制剂组(EA+ 2ME2).CON组、2ME2组、EA组及EA+ 2ME2组动物均建立大脑中动脉阻闭模型(MCAO),Sham组动物仅接受同前手术操作;EA组及EA+ 2ME2组大鼠接受连续5d电针刺激后24 h建立MCAO模型;2ME2组及EA+ 2ME2组动物分别于MCAO模型制备前30 min腹腔注射16 mg/kg的2ME2.缺血再灌注后24 h,各组随机抽取8只动物处死,行TUNEL染色检测神经元凋亡,Western Blot检测缺血半暗带中Bcl2/Bax的表达;缺血再灌注后72 h,各组另8只动物接受神经功能学评分后行磁共振成像(MRI)检查,随后处死行TTC染色检测脑梗死容积.结果:EA组脑梗死容积百分比显著低于CON组(P＜0.05);与CON组比较,EA组神经功能评分显著改善(P＜0.05),而2ME2可以显著降低EA+ 2ME2组神经功能评分(P＜0.05).与CON组比较,EA组神经功能评分显著改善(P＜0.05),而2ME2可以显著降低EA+ 2ME2组神经功能评分(P＜0.05).而CON组及EA+ 2ME2组中TUNEL阳性细胞显著多于EA组(P＜0.05).与EA组比较,CON组及EA+ 2ME2组中Bcl-2蛋白表达显著降低(P＜0.05),而CON组中Bax蛋白表达显著增加(P＜0.05).结论:电针预处理百会穴对脑缺血再灌注损伤具有明显的保护作用,其机制可能是HIF-1α抑制缺血后神经凋亡、上调凋亡抑制蛋白Bcl-2表达、下调促凋亡蛋白Bax表达,达到脑缺血保护的作用.

AimCarbon monoxide (CO) poisoning can cause permanent damage in tissues that are sensitive to hypoxia. We explored the feasibility and efficacy of using a hyperoxygenated solution (HOS) to treat severe acute CO poisoning in an animal model. MethodsMale Sprague-Dawley rats were subjected to CO poisoning. The HOS was administered into the femoral vein of these rats through a catheter (10 ml/kg). Carboxyhemoglobin (COHb) and blood gases were used to assess the early damage caused by CO poisoning. S100β was measured to predict the development of late cognitive sequelae of CO. The Morris water maze test was performed to assess cognitive function, and Nissl staining was performed to observe histologic change. ResultsThe COHb concentrations rapidly decreased at 5 min after the HOS administration; however, the PaO2 and SaO2 in rats treated with HOS increased significantly 5 min after the HOS administration. The S100β concentrations, which increased significantly after CO poisoning, increased at a much slower rate in the rats treated with HOS (HOS group) compared with the rats treated with O2 inhalation (O2 group). The escape latency in the place navigation test was shortened after CO poisoning on days 11-15 and days 26-30, and the swimming time in quadrant 4 in the spatial probe test on days 15 and 30 after CO poisoning was prolonged in the rats treated with HOS injection compared with the rats treated with oxygen inhalation or normal saline injection. The neuronal degeneration in the HOS group was alleviated than that in the CO or O2 group. ConclusionHOS efficiently alleviates the brain damage in acute CO-poisoned rats and thus may serve as a new way to treat human patients with CO poisoning in clinical practice.

目的:观察右美托咪啶（Dexmedetomidine,Dex）用于颌面外科清醒纤维支气管镜插管镇静的临床效果。方法:选择40例颌面外科手术患者,采用随机数分组:A组为右美托咪啶组,B组为咪达唑仑+芬太尼组,每组各20例。A组给予右美托咪啶1μg/kg,静脉泵注10 min、速度为6μg/（kg.h）;B组咪达唑仑2 mg+芬太尼0.05 mg静脉推注,当患者警觉/镇静（OAA/S）评分达3分,BIS值小于85时,应用1%利多卡因喷雾实施完善的上呼吸道表面麻醉,随后开始纤维支气管镜插管。观察比较2组给药前（T0）,镇静程度达3分,BIS小于85时（T1）,气管插管成功即刻（T2）和气管插管后5 min（T3）的OAA/S评分、心率（HR）、血压（BP）、脉搏氧饱和度（SPO2）、脑电双频指数（BIS）,T0和T3时血浆中去甲肾上腺素（NE）和肾上腺素（E）浓度,T1时右美托咪啶用药量,以及患者对插管的合作度和遗忘率。结果:A组用药后心率明显减慢且低于B组（P＜0.05）;插管后2组血压与T0比较都升高（P＜0.05）;用药后2组SPO2都下降,但A组明显高于B组（P＜0.05）;2组NE、E水平明显升高,但A组低于B组（P＜0.05）。结论:单独给予右美托咪啶可以产生良好的镇静镇痛效应,能明显抑制插管引起的应激反应,可单独辅助清醒纤维支气管镜插管,但需注意心动过缓的发生。

Nanosized hemoglobin-based oxygen carriers are one of the most promising blood substitutes. In the present study, a comprehensive strategy for the preparation of nanosized cationic amylose-encapsulated hemoglobins (NCAHbs) was developed. First, cationic amylase (CA) was synthesized from amylose and quaternary ammonium salt by an etherification reaction. The structure of CA was characterized using Fourier transform infrared spectrophotometry (FTIR) and proton nuclear magnetic resonance spectrophotometry (H-1 NMR). The degree of substitution and the zeta potential were also measured. Then, the NCAHbs were prepared by electrostatic adhesion, reverse micelles and cross-linking. The UV-visible spectrophotometer was used to measure the entrapment efficiency (EE%) and drug loading efficiency (DL%) of the NCAHbs. Transmission electron microscopy and Malvern Nano-zs 90 analyzer were used to observe the size distribution and morphology of particles. Chemical structure was determined from the FTIR spectrum. A Hemox analyzer was used to measure the P-50 and Hill coefficients. A lethal hemorrhagic shock model in rats was used to evaluate the therapeutic effect of the NCAHbs. The results showed that the combined methods improved the size, stability, EE%, DL%, and oxygen-carrying capacity of the NCAHbs. The average diameter of the NCAHbs was 92.53 +/- 3.64 nm, with a narrow polydispersity index of 0.027. The EE% was 80.05% +/- 1.56% and DL% was 61.55% +/- 1.41%. The P50 and Hill coefficient were equal to 28.96 +/- 1.33 mmHg and 2.55 +/- 0.22, respectively. The size of NCAHbs remained below 200 nm for six days in PBS solution. The NCAHbs could effectively prevent lung injury from progressing to lethal hemorrhagic shock because they acted as both a volume expander and an oxygen carrier. (C) 2011 Elsevier Ltd. All rights reserved.

Objective We used ischemic preconditioning method by blocking rabbit's right carotid artery at intervals repeatedly and increasing blocking time to reconstruct collateral circulation. Cerebral protection effects were investigated after the right carotid artery was permanently blocked. Methods 48 rabbits were randomly divided into experimental and control groups (n=24).The right common carotid artery of the animals in the experimental group was compressed at intervals repeatedly. We blocked the right carotid artery blood flow by the Inflatable balloon, ischemic time=number of times×5+40(min), 2 times per day. The longest blocking time is 4 h (20th days). The procedure of control group was the same as that of experimental group, except that the carotid artery blood flow was not blocked. The establishment of a right collateral circulation in the rabbit brain was observed with Digital Subtraction Angiography (DSA) on the 1st, 10th and 20th day respectively. The blood flow in the right common carotid artery was completely blocked at 20th day. The neurological deficit score was observed at 1, 3, 6, 24 h. Then we got brain tissue specimens and compared the brain water content and pathological changes between the two groups. The number of brain microvascular of the corresponding places was also counted. Results During the experiment, no abnormal behaviors such as excitement, agitation, lethargy were observed in either group. DSA showed that contrast medium passed into the right middle cerebral artery Willis ring on the 10th day.Compared with the 1st day, the blood vessels on the right side were much clearer in DSA. On the 20th day there was almost no difference between the left and right sides in vascular imaging. Experimental group's neurological deficit score and water content were lower than those of the control group's (P＜0.05). Observation showed that there were more brain microvascular in the right side (ischemic side) pathological specimens of the experimental group 5.3±0.5 than control group 3.5±0.4 (P＜O.05) under microscope at 400 times. Conclusion By multiple ischemic preconditioning cerebral artery Willis ring and cerebral collateral circulation would be reconstructed, and it had obvious protective effect on cerebral ischemia resulted from completely blocked carotid arteries.

Objective To investigate the effects of hyperoxygen solution(HOS)injected in vein on biochemical indexes of rats with acute carbon monoxide poisoning.Methods Eighteen SD rats were randomly divided into 3 groups,Normal group(N group),carbon monoxide poisoning group(C group)and HOS treatment groups(H15 group).Each contained 6 rats.After exposure of CO poisoning 1 h,C group accepted with balanced salt solution 15 ml/kg and H15 group with HOS 15 ml/kg.CO poisoning model were established by intraperitoneal injection CO with 120 ml/kg.C group and the treatment group were such poisoning rats,while N group were given the same dose of air.At the end of treatments,all the rats were collected 0.5 ml of arterial blood for blood gas measurement and 3 ml of venous blood for the determination of sensitive biochemical indexes in brain,heart,liver,and kidney.Results CO 120 ml/kg with intraperitoneal injection can cause severe hypoxemia after 1.5 h,PaO2 decreased from the(96.62 ± 2.4)nun Hg (1 mm Hg=0.133 kPa)to(43.04±4.13)mm Hg.After CO poisoning for 1 d,C group had test indicators increased significantly including neuron-specific enolase(NSE),troponin(cTnT),creatine kinase(CK),creatine kinase MB(CK-MB),lactate dehydrogenase(LDH),α-hydroxybutyrate dehydrogenase(ct-HBDH),total bilirubin(TBIL),aspartate aminotransferase(AST),alanine aminotransferase(ALT),glutamyl transferase(GGT),blood urea nitrogen(BUN)and creatinine(Cr)(P＜0.01).When intravenous infused with different doses of HOS,Dissolved oxygen in plasma was significantly increased,PaO2 increased from the (43.0± 4.1)mm Hg to(77.1±2.5)mm Hg.All the enzymes were significantly lower than these in C group,although still were significantly higher than these in N group(P＜0.01).Conclusion Intravenous infusion with HOS 15 ml/kg can reduce significantly the biochemical indexes changes caused by acute CO poisoning in rat,and prevent the importance organs from damage.