Isoflurane preserves energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation

AIM: To investigate the protective effect of isoflurane on energy balance in isolated hepatocytes during in vitro anoxia/reoxygenation, and to compare isoflurane with halothane. METHODS: Hepatocytes freshly isolated from fed rats were suspended in Krebs-Henseleit buffer, and incubated in sealed flasks under O2/CO2 or N2/CO2 (95%/5%, V/V) for 30 or 60 min, followed by 5 or 10 min of reoxygenation, with an added volatile anesthetic or not. ATP, ADP, and adenosine monophosphate in hepatocytes were determined by high performance liquid chromatography, and energy charge was calculated. RESULTS: During 30 min of anoxia, the energy charge and total adenine nudeotide steadily increased with the isoflurane dose from 0 to 2 minimum alveolar anesthetic concentration (MAC), then decreased from 2 to 3 MAC. In short incubations (30-35 min) at 1 MAC isoflurane, energy charge modestly decreased during anoxia, which was partially prevented by isoflurane and completely reversed by reoxygenation, and total adenine nudeotide did not decrease. In long incubations (60-70 min), both energy charge and total adenine nudeotide greatly decreased during anoxia, with partial and no reversal by reoxygenation, respectively. Isoflurane partly prevented decreases in both energy charge and total adenine nudeotide during anoxia and reoxygenation. In addition, 1 MAC isoflurane obviously increased ATP/ADP, which could not be changed by 1 MAC halothane. CONCLUSION: Isoflurane partially protects isolated hepatocytes against decreases in both energy charge and total adenine nudeotide during short (reversible) or long (irreversible) anoxia.

Effect of emulsified isoflurane on apoptosis of anoxia-reoxygenation neonatal rat cardiomyocytes

Objective:To explore the effect of emulsified isoflurane(EI)on apoptosis of anoxia-reoxygenation neonatal rat cardiomyocytea and relevant protein expression.Methods:Cardiac muscle anoxiareoxygenation damage model was established with culture in vitro neonatal rat cardiomyocytes.The cardiomyocytes were divided into control group,model group,fat emulsion group and EI group.The cardiomyocytes apoptosis rates and lactic dehydrogenase(LDH),superoxide dismutase(SOD)and malondialdehyde(MDA)index standardization were detected after relevant treatment The expression of apoptosis-related proteins Bel-2,Bax and Caspase-3 were detected with Western blot approach.Results:After hypoxia/reoxygenation(H/R)model was treated by EI,the cells apoptosis rate decreased and was dramatically below the fat emulsion group(P<0.05),Cardiomyocytes biochemical index detection presented that,compared with the control group that the LDH activity and MDA content dramatically increased(P<0.05),while the SOD activity notably decreased(P<0.05);compared with the H/R group,the SOD activity of the fat emulsion group and EI group increased(P<0.05);while the LDH activity and MDA content decreased(P<0.05).And the change of the EI group was more remarkable than the fat emulsion group(P<0.05).The Western blot analysis presented that,compared with the control group,the Bcl-2 protein expression of the other groups significantly decreased(P<0.05),the expressions of Bax protein and Caspase-3protein increased significantly(P<0.05);compared with H/R group,cardiomyocytes Bc1-2protein expression of EI group increased significantly(P<0.05),the expressions of Bax protein and Caspase-3 protein decreased significantly(P<0.05),and the change of EI group was more remarkable than the fat emulsion group(P<0.05).Conclusions:EI can inhabit the apoptosis of anoxia-reoxygenation damage model cardiomyocytes,and may he related to the up-regulation of expression of Bcl-2 and down-regulation of expression of Caspase-3 protein.

Rapamycin Protects Cardiomyocytes against Anoxia/Reoxygenation Injury by Inducing Autophagy through the PI3k/Akt Pathway

The purpose of this study was to investigate the potential cardioprotection roles of Rapamycin in anoxia/reoxygenation（A/R） injury of cardiomyocytes through inducing autophagy, and the involvement of PI3k/Akt pathway. We employed simulated A/R of neonatal rat ventricular myocytes（NRVM） as an in vitro model of ischemial/reperfusion（I/R） injury to the heart. NRVM were pretreated with four different concentrations of Rapamycin（20, 50, 100, 150 μmol/L）, and pretreated with 10 mmol/L 3-methyladenine（3MA） for inhibiting autophagy during A/R. Then, Western blot analysis was used to examine variation in the expression of LC3-Ⅱ, LC3-Ⅰ, Bim, caspase-3, p-PI3KⅠ, PI3KⅠ, p-Akt and Akt. In our model, Rapamycin had a preferential action on autophagy, increasing the expression of LC3-Ⅱ/ LC3-Ⅰ, whereas decreasing the expression of Bim and caspase-3. Moreover, our results also demonstrated that Rapamycin inhibited the activation of p-PI3KⅠ and enhanced the activation of p-Akt. It is concluded that Rapamycin has a cardioprotection effect by inducing autophagy in a concentration-dependent manner against apopotosis through PI3K/Akt signaling pathway during A/R in NRVM.

The antiapoptotic effect of insulin against anoxia/reoxygenation injury in cultured cardiomyocyte of neonatal rat

Objective： To study protective effect of insulin against cardiomyocyte apoptosis in anoxia/reoxygenation （A/R） injury of neonatal rat. Methods： The model of A/R injury was finished through receiving anoxia for 2h and reoxygenation for 4h in cultured cardiomyocytes of neonatal rat. The cardiomyocytes were divided randomly into 3 groups： control group （CON）, anoxia/reoxygenation group （A/R） and insulin-treated group （INS）. At the end of reoxygenation of 4 hours, activities of lactate dehydrogenase （LDH）, contents of malondiaidehyde （MDA）, were assessed through spectrophotometric procedures, myocyte apoptosis were detected through TUNEL and DNA Ladder. Results： MDA, LDH, and Apoptosis Index were significantly decreased in INS group compared with A/R group （P〈0.01）. Conclusion： Insulin has a protective effect against A/R injury in cultured cardiomyocyte of neonatal rat; the protective mechanism may contribute to antiapoptosis of insulin.

Ecological Devastation in Lake Victoria: Part A: Thermal Structure and Anoxia

Lake Victoria is the second (excl. Caspian Sea) largest lake in the world by surface area and 7th by Volume. The lake and catchment territories are shared between three countries, Kenya, Uganda and Tanzania. A research was carried out during 1990-1992 exploring the changes of the thermo-chemical structure occurred after the invasion of Nile Perch. Results of changes of physico-chemical (Temperature, DO and pH) conditions are summarized in this paper. The anoxic conditions by space and time were enhanced. Enhancement of pollutant supply from anthropogenic developments of terrestrial sources and atmospheric dust deposition accompanied by the deleterious effects of the Nile Perch invasion caused enhancement of anoxia in the lake in space and time. The combination of bottom-up nutrient supply and strong mixing conditions, expressed as low RTR values accelerate phytoplankton growth rate and production. The surplus of organic matter originated from algal biomass, enhanced anoxia.

Comparative insights into mitochondrial adaptations to anoxia in brain

Numerous diseases and pathologies impair the delivery of oxygen to brain, with rapid and deleterious consequences. For example, diseases related to systemic hypoxemia （e.g., chronic pulmonary disorders, cystic fibrosis）, decreased oxygen carrying capacity of blood （e.g., anemia）, or decreased transport （e.g., heart attack, stroke） can all reduce or entirely prevent the delivery of oxygen to brain cells, resulting in the initiation of programmed cell death pathways, necrosis, or excitotoxic cell death in brain （Pamenter, 2014）. However, oxygen-limited environments are common on earth and many organisms naturally experience periods of intermit- tent or prolonged hypoxia or anoxia in their daily and/or annual life cycles （Bickler and Buck, 2007）.

Epidemio-Clinical Characteristics of Perinatal Anoxia and Immediate Outcome of Patients at Hospital Teaching Gabriel Toure of Bamako

Introduction: Neonatal asphyxia (NA) is one of the most likely causes of neuro-developmental abnormalities in children. In Mali it is responsible for half of the early deaths and the third of neonatal mortality. Updated data would help understand and improve intervention strategies to reduce mortality. Objective: It is the study of epidemiological and clinical characteristics, the immediate outcome and the factors associated with newborn (NB) mortality with NA. Material and Methods: This was a prospective cross-sectional study from June 27th to September 3rd 2016 about the NBs admitted for NA in the Hospital Teaching Gabriel Touré of Bamako. The clinical and biological data including the prognosis were collected from the health records of women, the liaison sheets and the medical file. The analysis was done using the software Epi info version 3.5.1. Results: 76 NBs were included which represented 23.45% of hospitalizations. The majority (89.5%, n = 68) were admitted to less than 24 hours of life for NA grade III according to the Sarnat classification (43.4%, n = 33). The average age of mothers was 24.17 ± 5.5 years. Almost half (41.3%, n = 31) were primigravida. The most common obstetrical event was dystocia (64.5%, n = 49). The prognosis was poor in grade III anoxia in our patients (56%) of deaths. Conclusion: The périnatal anoxia (PA) is a major health issue in Mali because of its frequency and severity. Monitoring of pregnancies, delivery assisted by skillful and qualified personnel, mastery of neonatal resuscitation techniques are good means of prevention.

红景天苷防治眼科疾病的研究进展

红景天苷是从红景天分离得到的一种苯丙素苷,具有耐缺氧、抗氧化、抗炎、保护神经、抗疲劳、抗衰老及调节免疫等广谱药理特性。红景天苷具有多靶点—多途径的整体调节特征,通过激活磷脂酰肌醇-3-激酶/蛋白激酶B信号通路和单磷酸腺苷活化蛋白激酶途径、B淋巴细胞瘤-2基因/B淋巴细胞瘤-2基因相关X蛋白通路和内源性抗氧化酶的活性及环氧合酶/前列腺素E2信号通路保护糖尿病性视网膜病变视网膜血管内皮细胞、视网膜色素上皮细胞及Müller细胞;激活调控转化生长因子信号通路、磷脂酰肌醇-3-激酶/蛋白激酶B信号通路和分泌性糖蛋白/β-连环蛋白通路,从而抑制青光眼小梁网细胞和神经节细胞凋亡,并调节眼内压的稳定;激活蛋白激酶B/糖原合成酶激酶-3信号通路抑制年龄相关性黄斑变性视网膜色素上皮细胞氧化损伤,降低血管内皮生长因子和缺氧诱导因子-1的表达水平抑制脉络膜新生血管的形成;发挥抗氧化活性,保护白内障晶状体上皮细胞免受氧化损伤;改善近视所致的巩膜缺氧;以及通过激活单磷酸腺苷活化蛋白激酶—沉默信息调节因子1信号通路促进自噬等来抑制机体氧化应激,缓解干眼症引起的角膜上皮细胞氧化损伤等。红景天苷在眼科应用研究涉及的范围越来越广,本文就国内、外红景天苷治疗相关眼科疾病的最新研究进展予以综述。

槲芪方加减对肝癌化疗栓塞术后大鼠一氧化氮合酶、血管内皮生长因子、乏氧及免疫功能的影响

目的:研究槲芪方加减对肝癌化疗栓塞术后大鼠一氧化氮合酶(iNOS)、血管内皮生长因子(VEGF)、乏氧及免疫功能的影响。方法:50只大鼠中随机抽取12只作为健康组进行对照,37只大鼠建立肝癌模型。建模过程中意外死亡1只大鼠,剩余36只大鼠建模成功,随机分为模型组、肝动脉化疗栓塞术组以及联合组,每组12只。肝动脉化疗栓塞术组给予肝动脉化疗栓塞术(TACE)治疗;联合组在肝动脉化疗栓塞术组基础上给予模型大鼠27 ml/kg槲芪方灌胃,2次/d,共24周。运用全自动生化分析仪检测各组大鼠肝功能指标水平,流式细胞仪检测各组大鼠免疫功能指标水平,苏木精-伊红(HE)染色观察各组大鼠肝组织病理变化,原位末端标记法(TUNEL)检测各组大鼠肝癌细胞凋亡,免疫印迹检测各组大鼠VEGF、iNOS、缺氧诱导因子1α(HIF-1α)蛋白表达。结果:与健康组比较,模型组丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)水平均升高(P<0.05),与模型组比较,肝动脉化疗栓塞术组ALT、AST、ALP水平均降低(P<0.05),肝动脉化疗栓塞术组ALT、AST、ALP水平均高于联合组(P<0.05)。与健康组比较,模型组CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)降低,CD8^(+)升高(P<0.05),模型组与联合组比较差异无统计学意义(P>0.05),与模型组及联合组比较,肝动脉化疗栓塞术组CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)降低,CD8^(+)升高(P<0.05)。与健康组比较,模型组细胞凋亡率升高(P<0.05),与模型组比较,肝动脉化疗栓塞术组细胞凋亡率降低(P<0.05),肝动脉化疗栓塞术组细胞凋亡率低于联合组(P<0.05)。与健康组比较,模型组VEGF、iNOS、HIF-1α表达均升高(P<0.05),与模型组比较,肝动脉化疗栓塞术组VEGF、iNOS、HIF-1α表达均升高(P<0.05),与肝动脉化疗栓塞术组比较,联合组VEGF、iNOS、HIF-1α表达均降低(P<0.05)。结论:槲芪方加减可提高肝癌TACE术后大鼠的免疫功能,通过抑制肝癌大鼠乏氧微环境中HIF-1α、iNOS及VEGF水平,改善乏氧微环境,促进肿瘤细胞凋亡。

牛磺酸生产废水处理工程案例

湖北某牛磺酸生产企业废水处理工程,从企业生产工艺和废水水质特点出发,有针对性地采用“水解酸化+前缺氧+好氧生化+后缺氧+二沉”工艺处理该企业生产废水。进水平均COD、氨氮、总氮分别为956.8、50.6、99.1mg/L时,出水平均COD、氨氮、总氮分别为73.6、1.6、12.2 mg/L,COD、氨氮、总氮平均去除率可分别达到92.3%、96.9%、87.7%,出水水质稳定,达到《化学合成类制药工业水污染物排放标准》(GB 21904—2008)中新建企业水污染物排放浓度限值。采用渐减曝气和风机变频控制,能耗显著降低,单位水量运行费用为1.60元/m~3。

CircACAP2靶向miR-29a-3p/CCNT2轴对缺氧/复氧诱导的心肌细胞损伤的影响

目的:探讨CircACAP2靶向miR-29a-3p/细胞周期蛋白T2(CCNT2)轴对缺氧/复氧(H/R)诱导的心肌细胞损伤的影响。方法:将H9c2细胞分为Control组(正常培养)、si-NC组(转染si-NC)、Model组(建立H/R模型)、si-CircACAP2组(转染si-CircACAP2)、si-CircACAP2+inhibitor-NC组(si-CircACAP2和inhibitor-NC共转染)、si-CircACAP2+miR-29a-3p inhibitor组(si-CircACAP2和miR-29a-3p inhibitor共转染);实时荧光定量聚合酶链式反应(qRT-PCR)检测H9c2细胞中CircACAP2、miR-29a-3p的表达水平;四唑盐(MTT)法检测H9c2细胞活力;流式细胞仪检测H9c2细胞凋亡;单丹磺酰尸胺(MDC)染色法检测H9c2细胞自噬;乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)试剂盒检测H9c2细胞上清中LDH、MDA、SOD水平,DCFH-DA荧光探针法检测细胞内活性氧(ROS)水平;蛋白质免疫印迹法(Western Blot)检测增殖细胞核抗原(PCNA)、细胞凋亡蛋白[B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)]、自噬相关蛋白(Beclin-1、P62)及CCNT2的表达;双荧光素酶报告检测CircACAP2对miR-29a-3p的靶向关系和miR-29a-3p对CCNT2的靶向关系。结果:与Control组比较,Model组H9c2细胞中CircACAP2表达、凋亡率、自噬囊泡数、LDH释放率、MDA、ROS水平、Bax、Beclin-1、CCNT2蛋白表达升高,miR-29a-3p表达、OD490值、SOD活性、PCNA、Bcl-2、P62蛋白表达降低(P<0.05);与Model组比较,si-CircACAP2组H9c2细胞中CircACAP2表达、凋亡率、自噬囊泡数、LDH释放率、MDA、ROS水平、Bax、Beclin-1、CCNT2蛋白表达降低,miR-29a-3p表达、OD490值、SOD活性、PCNA、Bcl-2、P62蛋白表达升高(P<0.05);与si-CircACAP2组比较,si-CircACAP2+miR-29a-3p inhibitor组H9c2细胞中CircACAP2表达差异无统计学意义(P>0.05),凋亡率、自噬囊泡数、LDH释放率、MDA、ROS水平、Bax、Beclin-1、CCNT2蛋白表达升高,miR-29a-3p表达、OD490值、SOD活性、PCNA、Bcl-2、P62蛋白表达降低(P<0.05);CircACAP2靶向调控miR-29a-3p的表达,miR-29a-3p靶向负调控CCNT2的表达。结论:敲低CircACAP2可能通过靶向miR-29a-3p来下调CCNT2表达,进而抑制H/R诱导的H9c2细胞凋亡、自噬能力及氧化应激,促进细胞增殖,发挥保护作用。

MRI扩散加权成像对急性脑梗死患者神经损伤程度的评估价值

目的:探究磁共振成像(magnetic resonance imaging,MRI)扩散加权成像(diffusion weighted imaging,DWI)对急性脑梗死患者神经损伤程度的评估价值。方法:回顾性选取2021年9月—2023年8月苏州市相城人民医院收治的150例急性脑梗死患者。根据NIHSS评分将其分为轻-中度组(65例)和重度组(85例)。两组均进行常规MRI检查和DWI检查。比较两组表观弥散系数(apparent diffusion coefficient,ADC)和相对表观扩散系数(relative apparent diffusion coefficient,rADC)、梗死病灶梗死体积和FLAIR血管高信号(FLAIR vascular hyperintensity,FVH)征评分。分析梗死体积、FVH征评分、ADC和rADC与急性脑梗死严重程度的相关性。分析梗死体积、FVH征评分、ADC对急性脑梗死患者病情严重程度的诊断价值。结果:重度组ADC与rADC均高于轻-中度组,差异有统计学意义(P<0.05)。重度组FVH征评分和梗死体积均高于轻-中度组,差异有统计学意义(P<0.05)。梗死体积、FVH征评分、ADC及rADC均与疾病严重程度呈正相关(P<0.001)。结论:MRI DWI对急性脑梗死患者神经损伤程度评估的准确度和敏感度高,具有较高诊断价值。

鼻塞式持续气道正压通气对小儿重症肺炎治疗效果与安全性分析

目的对于重症肺炎患儿,鼻塞式持续气道正压通气的临床疗效和安全性进行探讨研究。方法回顾性收集100例2021年1月至2024年1月石狮市妇幼保健院收治的重症肺炎患儿临床资料,根据所采取治疗方案的不同将其分为观察组(鼻塞式持续气道正压通气)和对照组(鼻导管吸氧),每组患儿均为50例。比较两组患儿临床疗效、临床相关症状缓解时间、血气相关指标、生命体征相关指标、PCIS评分以及安全性。结果两组患儿治疗后临床总有效率观察组显著高于对照组(P<0.05)。观察组患儿心率降至正常、呼吸困难缓解以及肺部啰音消失所需时间均较对照组患儿短(P<0.001)。治疗前,两组患儿的PaO_(2)、PaCO_(2)、SaO_(2)水平,呼吸频率和心率以及PCIS评分均无显著差异(P>0.05);治疗后,两组患儿以上指标水平均改善,且观察组患儿PaO_(2)、SaO_(2)水平、PCIS评分显著高于对照组(P<0.05);PaO_(2)、PaCO_(2)、呼吸频率和心率显著低于对照组(P<0.05),观察组患儿不良反应总发生率与对照组比较差异无统计学意义(P=0.002)。结论对于重症肺炎患儿,早期给予鼻塞式持续气道正压通气,可有效缩短临床症状缓解所需时间,纠正缺氧状态,提高临床疗效,安全性高。

硫化氢——心血管功能调节的新型气体信号分子

Hydrogen sulfide (H 2S) may be endogenously produced by cystathionine β lyase (CBS) and cystathionine γ lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H 2S concentration, the gene expression and the activity (CSE) were decreased in lung tissues In L -NAME induced hypertension and spontaneous hypertension rats (SHR) models, the plasma H 2S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H 2S was exogenously supplied, systolic pressure obviously decrease. These studies suggested that CSE/H 2S pathway participated in the pathophysiological development of hypertension. The endogenous level of H 2S produced by some arterial tissues increased in both septic and endotoxic shock rats. The level of H 2S highly correlated with the endogenous level of NO These results suggest that H 2S may be a novel cardiovascular functional regulator.

新型气体信号分子硫化氢对低氧大鼠肺动脉平滑肌细胞凋亡的影响

目的 :探讨新型气体信号分子硫化氢 (H2 S)对低氧大鼠肺动脉平滑肌细胞凋亡的调节作用。方法 :2 4只Wistar大鼠 ,随机分为对照组 (8只 )、低氧组 (8只 )和低氧 +NaHS组 (8只 )。以化学分光光度法测定血浆H2 S含量 ;采用原位缺口末端标记方法 (TUNEL)检测大鼠肺动脉平滑肌细胞的凋亡 ,并行图像分析计算单位面积细胞凋亡率 ;采用免疫组织化学方法检测肺动脉平滑肌细胞凋亡蛋白Bcl 2、Fas和caspase 3表达 ,并进行定位和半定量分析。结果 :低氧组与对照组比较 ,低氧组大鼠血浆中H2 S含量下降 36 % ,应用TUNEL检测肺动脉平滑肌细胞单位面积凋亡率减少 5 2 .9% ,肺动脉平滑肌细胞Bcl 2蛋白表达增高 1 2 3.9% ,Fas蛋白表达减弱 4 5 % ,caspase 3表达与对照组差异无显著性 ;低氧组与低氧 +NaHS组比较 ,低氧 +NaHS组大鼠血浆中H2 S含量升高 6 5 % ,应用TUNEL检测到肺动脉平滑肌细胞单位面积凋亡率较低氧组增高 6 2 .5 % ,肺动脉平滑肌细胞Bcl 2蛋白表达减弱 36 .4 % ,Fas和caspase 3蛋白表达分别增高 84 .8%、34.5 % ;结论 :低氧时肺动脉平滑肌细胞凋亡减少 ,H2 S可能通过抑制肺动脉平滑肌细胞Bcl 2蛋白表达、增加Fas和caspase 3蛋白表达 。

安宫牛黄丸及其简化方的药效学比较研究

目的:根据安宫牛黄丸的治疗学作用,比较研究安宫牛黄丸及其简化方(安宫牛黄丸全方仅缺朱砂和雄黄)的药效学作用,以探讨安宫牛黄丸中朱砂和雄黄对其药效作用的影响。方法:实验以伤寒菌苗致家兔发热、戊巴比妥钠诱导小鼠睡眠、NaNO_2诱导小鼠缺氧死亡、硝酸士的宁及戊四唑诱发小鼠惊厥为模型,观察比较安宫牛黄丸及其简化方的药效学作用。结果:安宫牛黄丸及其简化方有明显的解热作用;安宫牛黄丸及其简化方与戊巴比妥钠有明显的协同镇静作用;对NaNO_2诱导的小鼠缺氧死亡有明显的保护作用;安宫牛黄丸及其简化方对硝酸士的宁及成四唑诱发小鼠惊厥无明显的保护作用。结论:安宫牛黄丸及其简化方在上述药效学研究中,两者在药效学上无明显差异。

鹿茸多肽对小鼠耐缺氧和抗疲劳能力的影响

实验观察鹿茸多肽(piloseantlerpolypeptide,PAP)对小鼠耐缺氧和抗疲劳能力的影响。实验设立对照组和实验组(PAP低剂量、中剂量和高剂量组),其中实验组灌胃给予高、中、低剂量的PAP,对照组灌胃给予同低剂量PAP组相同体积的生理盐水。连续灌胃30d,常压耐缺氧法观察小鼠存活时间,断头缺氧缺血法观察小鼠张口喘气时间,并观察小鼠爬杆时间、负重游泳时间,测定游泳前、游泳后0min和20min血清乳酸含量的变化。结果显示PAP能显著增加小鼠常压缺氧存活时间、断头喘气时间、爬杆时间和负重游泳时间;并能显著降低游泳后血清乳酸的增加量。说明PAP能够提高小鼠耐缺氧和抗疲劳的能力。

厚朴酚对脑缺血的保护作用

目的 研究厚朴酚对脑缺血的保护作用。方法 采用小鼠常压耐缺氧实验 ,测定小鼠氧耗量及存活时间 ;小鼠双侧颈总动脉结扎引起急性不完全脑缺血模型 ,测定小鼠死亡时间 ;大鼠大脑中动脉阻塞法 (MCAO)造成局灶性脑缺血模型 ,评价动物行为功能 ,测定脑梗死范围及脑组织中SOD、MDA及LDH的含量 ,并进行病理学组织检查。结果 厚朴酚能剂量依赖性地延长小鼠缺氧缺血的存活时间 ;改善大鼠脑缺血造成的行为缺陷 ,提高脑组织中SOD和LDH活性 ,减少MDA含量 ,缩小梗死范围 ,降低脑含水量。病理学组织检查显示 ,厚朴酚能改善脑缺血造成的大鼠神经细胞的损伤 ,减少组织坏死。结论 厚朴酚对脑缺血有保护作用 。

急性重型颅脑损伤患者预后的影响因素(英文)

目的 :探讨 GCS评分、年龄、低氧血症、高热和颅内高压对 84 6例急性重型颅脑损伤患者预后的影响。方法 :对我科84 6例急性重型颅脑损伤患者预后的影响因素进行回顾性分析。 结果 :84 6例急性颅脑损伤患者中 ,恢复良好 3 1 .56%、中残1 4.0 7%、重残 2 4 .3 5%、植物生存 0 .59%、死亡 2 9.4 3 %。GCS评分、年龄、低氧血症、高热、颅内高压与患者预后有明显相关( P<0 .0 1 )。 结论 :低氧血症、高热、颅内高压是导致患者死残的主要原因 ,防治低氧血症、降低颅内压、防治高热和亚低温治疗能有效地改善重型颅脑损伤患者的预后。

人参皂苷Rb_1对大鼠胎鼠海马神经细胞凋亡的影响

目的 :以原代培养的大鼠胎鼠海马神经细胞缺氧 /缺糖再给氧为模型 ,观察人参皂苷Rb1对神经细胞凋亡的抑制作用。方法 :流式细胞术检测凋亡细胞百分率 ,荧光显微镜观察细胞形态学变化和坏死细胞百分率 ,同时 ,测定细胞LDH的释放和NO的产生量。结果 :神经细胞缺氧 /缺糖 5h后再给氧可诱导神经细胞凋亡和细胞坏死 ,并显著增加LDH的释放和NO的产生 ,并随再给氧时间的延长而增加。人参皂苷Rb1能降低神经细胞凋亡及坏死的百分率 ,减少LDH的释放和NO的过量产生 ,人参皂苷Rb1的作用随剂量增加而作用增加。结论 :人参皂苷Rb1具有拮抗海马神经细胞凋亡的作用 ,这种作用可能与降低或抑制NOS活性 ,减少NO的过量产生有关。