Objective:To explore the effect of SimMan 3G simulator based scenario simulation teaching method and case-based learning (CBL) in emergency medicine teaching.Methods:Sixty students from Batch 2013 eight-year program of clinical medicine were selected as subjects. They were randomly divided into an experimental group and a control group, with 30 students in each group. In the teaching of emergency medicine, the experimental group used the combination of scenario simulation with CBL teaching methods, and the control group used classic teaching methods. The test scores and the questionnaires satisfaction of the two groups were compared to evaluate the teaching effects. SPSS 17.0 was used for the statistical analysis, measurement data were compared between the groups by t test, and counting data were compared between groups by chi-square test.Results:The scores of the experimental group (94.24±1.13) were better than those of the control group (90.6±0.59), with significant differences ( t=12.85, P<0.05). The results of the questionnaires showed that the students of experimental group were more satisfied with the learning experience than those of the control group. Conclusion:The teaching method can improve the teaching effects, the students' emergency clinical thinking, skills, comprehensive analysis and judgment ability, team cooperation consciousness and leadership ability.

Cardiac arrest (CA) yields poor neurological outcomes. Salubrinal (Sal), an endoplasmic reticulum (ER) stress inhibitor, has been shown to have neuroprotective effects in both in vivo and in vitro brain injury models. This study investigated the neuroprotective mechanisms of Sal in postresuscitation brain damage in a rodent model of CA. In the present study, rats were subjected to 6 min of CA and then successfully resuscitated. Either Sal (1 mg/kg) or vehicle (DMSO) was injected blindly 30 min before the induction of CA. Neurological status was assessed 24 h after CA, and the cortex was collected for analysis. As a result, we observed that, compared with the vehicle-treated animals, the rats pretreated with Sal exhibited markedly improved neurological performance and cortical mitochondrial morphology 24 h after CA. Moreover, Sal pretreatment was associated with the following: (1) upregulation of superoxide dismutase activity and a reduction in maleic dialdehyde content; (2) preserved mitochondrial membrane potential; (3) amelioration of the abnormal distribution of cytochrome C; and (4) an increased Bcl-2/Bax ratio, decreased cleaved caspase 3 upregulation, and enhanced HIF-1α expression. Our findings suggested that Sal treatment improved neurological dysfunction 24 h after CPR (cardiopulmonary resuscitation), possibly through mitochondrial preservation and stabilizing the structure of HIF-1α.

Brain damage is a leading cause of death in patients with cardiac arrest (CA). The accumulation of succinate during ischemia by succinate dehydrogenase (SDH) is an important mechanism of ischemia-reperfusion injury. It was unclear whether inhibiting the oxidation of accumulated succinate could also mitigate brain damage after CA. In this study, rats were subjected to a 6 min of CA, and cardiopulmonary resuscitation (CPR) was performed with administration of normal saline or dimethyl malonate (DMM, a competitive inhibitor of SDH). After the return of spontaneous circulation, neurological function of the rats was assessed by a tape removal test for 3 days. The rats were then sacrificed, and their brains were used to assess neuronal apoptosis by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Hippocampal tissues were used for Western blotting analysis and biochemical detection. In addition, hippocampal mitochondria during CA and CPR were isolated. The relative mitochondrial membrane potential (MMP) and cytochrome C in the cytosol were detected. Our results show that DMM promoted ROSC and neurological performance in rats after CA. The TUNEL assay showed that DMM reduced neuronal apoptosis. Western blotting analysis showed that DMM inhibited the activation of caspase-3 and enhanced the expression of HIF-1 alpha. Moreover, DMM inhibited excessive hyperpolarization of MMP after CPR, and prevented the release of cytochrome C. Therefore, inhibiting SDH by DMM alleviated brain damage after CA, and the main mechanisms included inhibiting the excessive hyperpolarization of MMP, reducing the generation of mtROS and stabilizing the structure of HIF-1 alpha. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

暴发性心肌炎(fulminant myocarditis,FM)起病症状轻,病情进展迅速,往往在几天之内迅速出现心原性休克,甚至并发多器官功能衰竭.本文报道1例暴发性心肌炎合并多器官功能衰竭病例,探讨暴发性心肌炎的早期诊断方法及治疗方案. 病例资料 患者男,43岁,因“胸闷乏力7d,加重3d”于2017年1月10日入院.患者于2017年1月4日夜间自觉畏冷乏力,自行以感冒治疗2d,效果不佳,感觉胸闷乏力症状加重,2d后就诊于荆门市第一人民医院,查肌钙蛋白(cTnI) 1609.0 pg/mL,B型钠尿肽前体(NT-proBNP) 29600.0 pg/mL,胸片示:双肺渗出,双侧胸腔少量积液;小叶间隔广泛增厚,提示间质性改变;心包少量积液;胆囊炎,考虑重症心肌炎,予以抗感染、抗病毒、营养心肌、利尿、维持心功能等治疗.次日,患者血氧饱和度下降,给予气管插管呼吸机辅助呼吸,病情危重,于2017年1月10日来华中科技大学同济医学院附属同济医院就诊.入院查体:T 37.3℃,P 122次/min,R25次/min,BP79/49 mmHg(大剂量升压药维持).辅助检查:血WBC 9.90×109/L,N％ 87.3％,N 3.86×109/L,RBC3.99×1012/L,Hb 105.0 g/L,PLT 146×109/L,ALT4749 U/L,AST＞7 000 U/L,ALB 25.8 g/L,TB32.0 μmol/L,CB 20.4 μmol/L,UCB 11.6 μmol/L,SCr334 μmol/L;凝血功能PT 22.6 s,INR 2.00,APTT78.1 s,TT 22.9 s,Lac 3.309 mmol/L;心脏超声:左室扩大并收缩功能降低(左室射血分数EF18％),少量心包积液.

目的 急性心肌梗死患者因为部分基层医院没有介入手术条件,需要转诊胸痛中心延迟接受急诊PCI,比较静脉溶栓后转运与直接转运胸痛中心时间窗内延迟介人治疗的临床疗效,改进因客观原因延迟PCI的抢救治疗流程而进一步改善部分患者的预后.方法 选取2015年1月-12月期间因为急性心肌梗死经华中科技大学同济医学院附属同济医院急救中心急救转入同济胸痛中心接受治疗的48例患者为研究对象,将其随机分为两组,观察组:24例采用转院前静脉溶栓后转诊胸痛中心急诊PCI,对照组24例没有接受溶栓直接转诊胸痛中心急诊PCI,分析两组患者的临床治疗效果.结果 对照组心电图检测ST段下移率为41.7%,胸痛明显缓解率为45.8%;观察组心电图检测ST段下移率为87.5%,胸痛明显缓解率为79.2%,两组患者治疗效果差异明显,P<0.05,差异有统计学意义.结论 临床上因部分基层医院没有介入手术条件,需要转诊胸痛中心延迟接受急诊PCI,客观原因延迟PCI的急性心肌梗死患者,转院外静脉溶栓后转诊比直接转诊延时PCI疗效明显,且安全性高,值得院外急救转诊推广研究.

Although therapeutic hypothermia is an effective treatment for post-resuscitation brain injury after cardiac arrest (CA), the underlying mechanism remains unclear. Vacuolar H(+)-ATPase (V-ATPase) plays a key role in cellular adaption to a hypoxic environment. This study sought to evaluate the effect of mild hypothermia on V-ATPase and its involvement in neuroprotection after CA. Male Sprague-Dawley rats were subjected to a 6-min CA, resuscitated successfully, and then assigned to either the normothermia (NT) group or the hypothermia (HT) group. Rats were further divided into 2 subgroups based on the time of euthanasia, either 3 or 24 h after CA (NT-3 h, HT-3 h; NT-24 h, HT-24 h). Mild hypothermia was induced following CA and maintained at 33°C for 2 h. Neurologic deficit scores were used to determine the status of neurological function. Brain specimens were analyzed by TUNEL assay, western blotting, and immunohistochemistry. V-ATPase activity was estimated by subtracting total ATP hydrolysis from the bafilomycin-sensitive activity. Mild hypothermia improved the neurological outcome (HT-24 h: 34.3 ± 16.4 vs NT-24 h: 50.3 ± 17.4) and significantly decreased neurocyte apoptosis 24 h after resuscitation. Mild hypothermia significantly increased V0a1 compared to NT-3 h; V0a1 expression was associated with a decrease in the cleaved caspase 3 expression. These findings suggested that mild hypothermia inhibits CA-induced apoptosis in the hippocampus, which may be associated with reduced V-ATPase impairment. These data provide new insights into the protective effects of hypothermia in vivo.

Objective To explore the effect of propofol pretreatment on postresuscitation brain protection in a rat model of cardiac arrest and the relationship with endoplasmic reticulum stress(ERS). Methods Forty-five male SD rats were randomly divided into Sham group(n=15), Intralipid group (n=15)and Propofol group(n=15). Rats of Sham group conducted all operations without induce of cardiac arrest. Rats of Intralipid group and Propofol group were operated to induce cardiac arrest by transcutaneous electrical stimulation to epicardium. In Propofol group, propofol(10 mg/kg)was adminis? trated via the intraperitoneal 30 min before operation. In Intralipid group, MCT/LCT(same volume of propofol)was administrated via the intraperitoneal 30 min before operation. The survival rats were ob?served 24 h after restoration of spontaneous circulation(ROSC)and neurological status was evaluated by neurological deficit score(NDS). 24 h after ROSC, brains were removed for analysis of hematoxylin-eo?sin(HE)staining, TUNEL assays and western-blot. Results Compared with the Sham group, the rats in Intralipid group and Propofol group have poorer neurological outcomes(P<0.05), varying degrees histopathological changes in the CA1 region of the hippocampus and higher apoptosis index(P<0.01). Compared with the Intralipid group, there was a significant improvement in NDS(P<0.05), histopatho?logical changes and apoptosis index(P<0.01)in Propofol group. The expressive protein of GRP78, XBP-1, CHOP and caspase12 in Intralipid group and Propofol group were higher than those in Sham group(P< 0.01). Compared with the Intralipid group, the Propofol group had lower expressive protein of XBP-1, CHOP and caspase12(P<0.01), but higher expression of GRP78 protein(P<0.01). Con-clusion Propofol pretreatment can mitigate brain injury after ROSC through inhibition of ERS.

Postcardiac arrest syndrome yields poor neurological outcomes, but the mechanisms underlying this condition remain poorly understood. This study investigated whether endoplasmic reticulum (ER) stress-mediated apoptosis is induced in injured brain after resuscitation. Sprague-Dawley rats were subjected to 6 min of cardiac arrest (CA) and then resuscitated successfully. In the first experiment, animals were sacrificed 1, 3, 6, 12, or 24 h (n = 3 per group) after successful cardiopulmonary resuscitation. Brain tissues were analyzed by real-time polymerase chain reaction and Western blotting. In the second experiment, either dimethyl sulfoxide or salubrinal (Sal; 1 mg/kg), an ER stress inhibitor, was injected 30 min before the induction of CA (n = 10 per group). Neurological deficits were evaluated 24 h after CA. Brain specimens were analyzed using electron microscopy, terminal deoxynucleotidyl transferase dUTP nick end labeling assays and immunohistochemistry. We found that the messenger RNA and protein levels of glucose-regulated protein 78, X-box binding protein 1, C/EBP homologous protein, and caspase 12 were significantly elevated after resuscitation. We also observed that rats treated with Sal exhibited an improved neurological deficit score (32.3 ± 15.5 in the Sal group vs. 49.8 ± 20.9 in controls, P < 0.05). In addition, morphological improvements in the hippocampal ER were observed in the Sal group compared with the dimethyl sulfoxide group 24 h after reperfusion. Furthermore, in situ immunostaining revealed that markers of ER stress were significantly inhibited by Sal pretreatment. Our findings suggested that ER stress and the associated apoptotic pathways were activated in the hippocampus after resuscitation. Administration of Sal 30 min before cardiopulmonary resuscitation ameliorated neurological dysfunction 24 h after CA, possibly through the inhibition of ER stress after postresuscitation brain injury.

Poor neurological outcome remains a major problem in patients with cardiac arrest. Ghrelin has been shown to be neuroprotective in models of neurologic injury in vitro and in vivo. This study was performed to assess the effects of ghrelin on postresuscitation brain injury in a rat model of cardiac arrest. Sprague-Dawley rats were subjected to 6-min cardiac arrest and resuscitated successfully. Either vehicle (saline) or ghrelin (80 μg/kg) was injected blindly immediately after return of spontaneous circulation (ROSC). A tape removal test was performed to evaluate neurological function at 24, 48, and 72 h after ROSC. Then, brain tissues were harvested and coronal brain sections were analyzed by hematoxylin and eosin (HE) staining for neuronal viability and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining for apoptosis in hippocampal CA1 sectors. In additional groups, rats were sacrificed at 6 h after ROSC, and hippocampal tissues were collected for further analysis. We found that animals treated with ghrelin had improved neurological performances, reduced neuronal injury, and inhibited neuronal apoptosis compared with the vehicle group. Moreover, ghrelin treatment was associated with the following: (1) a decrease in caspase-3 up-regulation and an increased Bcl-2/Bax ratio, (2) a reduction in maleic dialdehyde content and an up-regulation in superoxide dismutase activity, and (3) an increase in uncoupling protein 2 (UCP-2) expression. Our results suggest that ghrelin treatment attenuated postresuscitation brain injury in rats, possibly via regulation of apoptosis, oxidative stress, and mitochondrial UCP-2 expression. Ghrelin may have therapeutic potential when administered after cardiac arrest and cardiopulmonary resuscitation.

Objective To investigate the effects of exogenous hydrogen sulfide (H2S) on injury of rat hippocampus neurons induced by oxygen-glucose deprivation and restoration (OGD/R) and explore its mechanism.Methods Hippocampus neurons were isolated from embryonic day 16-18 (E16-18) rat embryos.Hippocampus was immediately removed and digested with 0.25％ trypsin.The neurons were isolated and cultured at 37 ℃ for 7 days and neuron-specific enolase (NSE) was detected by immunohistochemical staining method to identify neurons.At 8th day,the neurons were placed in deoxygenated glucose-free medium and exposed to 95％ N2-5％ CO2 in an air tight chamber for 1 hour,and then replaced the glucose-free medium with original medium,and returned the cultures to a standard incubator in 5％ CO2 at 37 ℃ and incubated for another 24 h.The neurons were divided into 3 groups:group Ⅰ control; group Ⅱ OGD/R,and group ⅢOGD + NaHS,the latter was further divided into 5 subgroups:groups Ⅲ1-5 with 25,50,100,200,400 μmol/L NaHS added,respectively.Then cell viability was quantified by MTT method,the level of lactate dehydrogenase (LDH) were detected,apoptosis was measured by Annexin V FITC/PI Apoptosis Kits,and RT-PCR was used to assay HIF-1 α mRNA in neurons in all groups.Results Compared with control group,the LDH level,apoptosis and expression of HIF-1α mRNA in group Ⅱ were significantly increased,the cell viability was significantly decreased (P ＜ 0.01).There were no significant differences in the LDH level,apoptosis and expression of HIF-1 α mRNA and the cell viability between group Ⅱ and group Ⅲ1 (P ＞ 0.05).Compared with group Ⅱ,the LDH level,apoptosis and expression of HIF-1α mRNA in group Ⅲ2-4 were significantly increased,the cell viability was significantly increased (P ＜ 0.01).Compared with group Ⅱ,the LDH level,apoptosis and expression of HIF-1 α mRNA in the group Ⅲ 5 were significantly decreased,the cell viability was significantly decreased (P ＜ 0.01).Conclusions H2S of low concentration has no significant effects on injury of rat hippocampus neurons induced by OGD/R.H2S of moderate doses can protect rat hippocampus neurons from OGD/R injury and H2S of high concentration can aggravate injury.The expression of HIF-1α mRNA in rat hippocampus neurons was increased after OGD/R,and the protective role of H2S is associated with increase in the expression of HIF-1α mRNA.

Mitochondrial dysfunction plays a critical role in brain injury after cardiac arrest and cardiopulmonary resuscitation (CPR). Recent studies demonstrated that hydrogen sulfide (H2S) donor compounds preserve mitochondrial morphology and function during ischemia-reperfusion injury. In this study, we sought to explore the effects of sodium hydrosulfide (NaHS) on brain mitochondria 24h after cardiac arrest and resuscitation. Male Sprague-Dawley rats were subjected to 6min cardiac arrest and then resuscitated successfully. Rats received NaHS (0.5mg/kg) or vehicle (0.9% NaCl, 1.67ml/kg) 1min before the start of CPR intravenously, followed by a continuous infusion of NaHS (1.5mg/kg/h) or vehicle (5ml/kg/h) for 3h. Neurological deficit was evaluated 24h after resuscitation and then cortex was collected for assessments. As a result, we found that rats treated with NaHS revealed an improved neurological outcome and cortex mitochondrial morphology 24h after resuscitation. We also observed that NaHS therapy reduced intracellular reactive oxygen species generation and calcium overload, inhibited mitochondrial permeability transition pores, preserved mitochondrial membrane potential, elevated ATP level and ameliorated the cytochrome c abnormal distribution. Further studies indicated that NaHS administration increased mitochondrial biogenesis in cortex at the same time. Our findings suggested that administration of NaHS 1min prior CPR and followed by a continuous infusion ameliorated neurological dysfunction 24h after resuscitation, possibly through mitochondria preservation as well as by promoting mitochondrial biogenesis.

Objective: Apoptosis and necrosis of neurons induced by hypoxia-ischemia and reperfusion are thought to be the main mechanisms of postresuscitation brain injury. Vacuolar H + -ATPase (V-ATPase) has been shown an essential role in the anti-oxidative and anti-apoptotic activities. 1 Milgrom E. Diab H. Middleton F. et al. Loss of vacuolar proton-translocating ATPase activity in yeast results in chronic oxidative stress. J Biol Chem. 2007; 282: 7125-7136 Crossref PubMed Scopus (80) Google Scholar , 2 Chung C. Mader C.C. Schmitz J.C. et al. The vacuolar-ATPase modulates matrix metalloproteinase isoforms in human pancreatic cancer. Lab Invest. 2011; 91: 732-743 Crossref PubMed Scopus (80) Google Scholar The aim of this study was to investigate changes in V-ATPase expression in the cerebrum after cardiopulmonary resuscitation (CPR) in a rat model.

Objective To explore the effects of hydrogen sulfide (H2S) on apoptosis of cardiomyocytes after cardiopulmonary resuscitation (CPR) in rat models.Methods Forty-five male SD rats were randomly into sham group (n =15),CPR group (n =15) and NaHS group (n =15).Rats of CPR group and NaHS group were operated to induce cardiac arrest by transcutaneous electrical stimulation to epicardium.In NaHS group,NaHS (5 mg/kg) was administrated via the femoral venous line 1 min before CPR.Hemodynamic variables were monitored and obtained continuously.Survival rats were sacrificed at 24 h after restoration of spontaneous circulation and the hearts were removed for analysis by RT-PCR and TUNEL assays.Blood samples were collected and plasma content of cTnT was detected.Results Compared with the CPR group,animals treated with NaHS had improved left ventricular function (P ＜0.01),lower plasma cTnT levels (P ＜0.05) and decreased apoptosis index (P ＜ 0.01) 24 h after ROSC.The expressions of Caspase-3 mRNA,Bax mRNA and Bcl-2 mRNA in CPR group and NaHS group were higher compared with the control group (P ＜0.01).The NaHS group had lower expressions of Caspase-3 mRNA and Bax mRNA (P ＜0.01),but higher expression of Bcl-2 mRNA (P ＜0.05) compared with the CPR group.Conclusions Exogenous (H2S) regulated the expressions of Caspase-3,Bax and Bcl-2 mRNA,thereby preventing apoptosis of cardiomyocytes,inhibiting cTnT release and improving left ventricular function 24 h after CPR.

The aim of this study was to observe the effects of different types of fluid resuscitation on hepatic mitochondria and apoptosis in hemorrhagic shock, and the corresponding mechanisms. Forty rats were divided into five groups: Sham surgery (Sham group), shock (Shock group), Ringer's lactate resuscitation (RL group), hydroxyethyl starch resuscitation (HES group) and autologous blood resuscitation (BL group). A model of hemorrhagic shock was successfully induced in the latter four groups. The recovery objective was to maintain the mean arterial pressure (MAP) of the rats at 80 mmHg. Two hours after the end of the recovery experiment, fresh liver samples were examined in order to observe the changes in the morphology and mitochondrial membrane potential (ΔΨm). In addition, the levels of succinate dehydrogenase (SDH) activity were assessed, and a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was conducted to evaluate the level of apoptosis in the liver cells. In the Shock, RL, HES and BL groups, mitochondrial ultrastructural damage in the liver cells, significant reductions in liver cell function, liver ΔΨm and SDH activity, and the apoptosis of hepatocytes were more apparent compared with those in the Sham group. In the BL group, compared with the RL and HES groups, the injuries to the mitochondrial ultrastructure and liver cell function were significantly reduced, the hepatic ΔΨm and SDH activity were significantly increased and the hepatocyte apoptosis index (AI) was significantly reduced (P<0.05). In conclusion, in a rat model of hemorrhagic shock, different methods of fluid resuscitation may improve the liver cells with regard to mitochondrial ultrastructure and function, the stability of liver ΔΨm, the activity of SDH and the inhibition of liver cell apoptosis. The results indicate that infusion with autologous blood followed by RL solution is a preferable method of fluid resuscitation compared with HES.

低钾血症是临床工作中常见的电解质紊乱之一，随着内分泌、代谢性疾病的增多和诊疗水平的提高，与之相关的低钾血症日益增多，肾小管酸中毒(RTA)是因近端肾小管HCO3-重吸收或远端肾小管泌 H+功能障碍引起的临床综合征。常伴低K+、高Cl-、代酸和尿pH增高。RTA 在临床上并非少见，但其缺乏特异性表现，易误诊为低 K+性周期性瘫痪、多发性肌炎、格林-巴利综合征等，目前临床上仍存在对内分泌、代谢性疾病相关性低钾血症病因及临床特点认识不足而导致的漏诊、误诊现象[1]。为总结经验教训，降低误诊率，现报道如下。

Aims: Cardiac arrest and cardiopulmonary resuscitation (CPR) can lead to intestinal ischemia/reperfusion (I/R) injury. Increasing studies have indicated that hydrogen sulfide (H2S) is in favor of a variety of tissue I/R injury. The purpose of this study was to explore whether sodium hydrosulfide (NaHS), a H2S donor, can protect intestinal mucosa after CPR and its potential mechanisms.Main methods: Male Sprague-Dawley rats were subjected to 6 min cardiac arrest induced by transcutaneous electrical epicardium stimulation and then resuscitated successfully. A bolus of either NaHS (0.5 mg/kg) or placebo (NaCl0.9%) was blindly injected 1 min before the start of CPR intravenously, followed by a continuous injection of NaHS (2 mg/kg/h) or placebo for 3 h. Intestinal and plasma samples were collected for assessments 24 h after CPR.Key findings: We found that NaHS can markedly alleviate cardiac arrest induced intestinal mucosal injury. Rats treated with NaHS showed a lower malondialdehyde content, higher superoxide dismutase activity and glutathione content in intestine after CPR. Increased intestinal myeloperoxidase activity was significantly decreased by NaHS after CPR. Moreover, a reduced intestinal apoptotic cells after CPR were evident when pretreated with NaHS. Further studies indicated that NaHS enhances the expression of hypoxia-inducible factor-1 alpha (HIF-1 alpha) in intestine after CPR.Significance: Our data demonstrated that NaHS treatment before CPR induces intestinal mucosal protection 24 h post-resuscitation. The protective effects may be through oxidative stress reduction, inflammation alleviation, apoptosis inhibition and HIF-1 alpha activation. (C) 2013 Elsevier Inc. All rights reserved.

Intestinal ischemia-reperfusion (I/R) is a critical event in the pathogenesis of multiple organ dysfunction syndromes (MODS). The lungs are some of the most vulnerable organs that are impacted by intestinal I/R. The aim of this study is to investigate whether ginsenoside Rb1 can ameliorate remote lung injury induced by intestinal I/R. Adult male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Intestinal and lung histology was observed. The malondialdehyde (MDA) levels in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-α, MDA levels, wet/dry weight ratio and immunohistochemical expression of intracellular adhesion molecule-1 (ICAM-1) in lung tissues were assayed. In addition, a western blot of lung NF-kB was performed. Results indicated that intestinal I/R induced intestinal and lung injury, which was characterized by increase of MDA levels and pathological scores in intestinal tissues and MPO, TNF-α , MDA levels, wet/dry weight ratio and ICAM-1, NF-kB expression in the lung tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated intestinal and lung injury, decreased MPO, TNF-α, MDA levels, wet/dry weight ratio, ICAM-1 and NF-kB expression in lung tissues. In conclusion, ginsenoside Rb1 ameliorated the lung injuries by decreasing the NF-kB activation-induced inflammatory response.

Objective: To analyze the clinical risk factors and potential etiologies of low cardiac output syndrome (LCOS) after heart valve replacement, and to provide the evidence for the clinical prevention and treatment. Methods: Three hundred and eighty-six patients with Swan-Ganz catheter monitoring after heart valve replacement were studied retrospectively, and they were divided into LCOS group and non-LCOS group. The risk factors related with LCOS in all cases were analyzed by logistic regression analysis. Results: One hundred and eight patients (28.0%)developed LCOS, while another 278 patients (72.0%) did not. There were no obvious differences in age, preoperative hypertension, diabetes, history of arrhythmia and way of valve replacement (P0.05). The preoperative body mass index of LCOS group was less than that of non-LCOS group, the cardiothoracic ratio, brain natriuetic peptide(BNP)and pulmonary arterial pressure(PAP), EuroSCORE rating were higher in LCOS group than those in non-LCOS group. The time of cardiopulmonary bypass and intraoperative aortic clamping were longer than those of non-LCOS group. The volume of postoperative blood loss and the subsequent second surgery were also more than those of non-LCOS group (P 0.05). Retrospective study demonstrated that preoperative BNP600 pg/mL, body mass index18 kg/m2, cardiothoracic ratio0.7, PAP65 mmHg, the time of CPB120 minutes, the time of aortic clamping60 minutes and postoperative blood loss 20% of total blood volume were the independent risk factors of developing LCOS after heart valve replacement. Combined with Swan-Ganz catheter monitoring data and auxiliary examination, such as bedside echocardiograph, we found that 62 cases (57.4%) with insufficient preload, 36 cases (33.3%) with pumping function failure, 6 patients (5.6%) with cardiac tamponade, 4 cases (3.7%) with arrhythmia leaded to postoperative LCOS. Conclusions: Preoperative heart failure, low body weight, cardiothoracic ratio0.7, pulmonary hypertension, the prolonged time of extracorporeal circulation and aortic clamping, massive blood loss are the risk factors of LCOS; preexisted load deficiency, heart failure, cardiac tamponade and arrhythmia are the main causes of LCOS.

OBJECTIVE To observe the effects and mechanisms of sodium tanshinone ⅡA sulfonate(STS) on angiotensin Ⅱ(Ang Ⅱ)-induced cardiomyocyte oxidative stress.METHODS In the primary culture of neonatal rat cardiomyocytes,the content of reactive oxygen species(ROS) was measured by 2,7-dichlorofluorescein diacetate(DCFH-DA).8-hydroxydeoxyguanosine level in the supernatant was measured by ELISA.As indexes of cardiomyocyte oxidative stress,the cellular contents of MDA and SOD,cell vialibity and LDH release were measured.NADPH oxidase(NOX) activity was measured by chromatometry.The expressions of p47 phox was assessed using Western blot.RESULTS STS can decrease Ang Ⅱ-induced elevations of ROS level and oxidative stress,and inhibit the expression of p47 phox and NOX activity.CONCLUSION The inhibitory effects of STS on Ang Ⅱ-induced cardiomyocyte oxidative stress may be associated with depressing NOX signaling pathway via down regulation of p47 phox expression.

Objective To investigate the protective effects of penehyclidine hvdrochloride (PHC)on lipopolysaccharide ( LPS)-induced human umbilical vein endothelial cells (HUVECs) injury and the underlying mechanism.Methods Cultured HUVECs were divided into five groups:control group,LPS group,LPS/PHC ( 10 μg/L) group,LPS/PHC (25 μg/L) group,LPS/PHC (50 μg/L) group.Cell viability was measured by methyl thiazol tetrazolium (MTT) colorimetric method.The concentrations of lactate dehydrogenase (LDH) and nitric oxide (NO) were measured respectively by using chemical colorimetric method and nitrate reduction method.The expression of inducible nitric oxide synthase (iNOS) mRNA and protein was detected hy using reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting respectively.The activity of nuclear factor-KB (NF-KB) and signal transducer and activators of transcription 3 (STAT3) were measured by enzyme linked immunosorbent assay (ELISA).Results As compared with control group,cell viability [(60.31 ± 8.76 )％ vs 100.00％] was decreased and the concentrations of LDH [(326 ±52) μmol/L vs ( 125 ±25) μmoL/L] and NO [(55.49 ± 10.16) μmol/L vs ( 12.13 ±11.02) μmol/L] were increased in LPS group ( P ＜0.01 ) ; PHC could revere these effects on HUVECs (P ＜0.05).At the same time,PHC reduced the expression of iNOS mRNA and protein,and the activity of NF-KB and STAT3 ( P ＜ 0.05 ).Conclusion PHC can protect the endothelial function by reducing the concentration of NO.Inhibiting the NF-KB and STAT3 signal pathway may be the underlying mechanism.