【 Abstract 】 Objective To investigate the effects of 250 ml/m3 carbon monoxide (CO) inhalation or intraperitoneal infusion on lipopolysaccharide (LPS) induced rat intestinal tract injury, and to detect the roles of p38 mitogen-activated protein kinase (MAPK) pathway during CO administration. Methods After received 5 mg/kg LPS or an equal volume of normal saline by intravenous injection, 108 male SD rats were randomly divided into 6 groups: control group, CO inhalation (250 ml/m3) group, CO intraperitoneal infusion (250 ml/m3 at a rate of 2 L/min) group, LPS (5 mg/kg) group, LPS (5 mg/kg)+CO inhalation (250 ml/m3) group and LPS (5 mg/kg)+CO intraperitoneal infusion (250 ml/m3 at a rate of 2 L/min) group. The animals were differently sacrificed at 1, 3 and 6 h for the observation, and the ileum tissues were homogenized for determination the levels of platelet activator factor (PAF), intercellular adhesion molecule-1 (ICAM-1) and interlukin-10 (IL-10) with enzyme-lined immunosorbent assay, the content of maleic dialdehyde (MDA) with thiobarbitric acid, the activity of myeloperoxidase (MPO) with chemical method, the activity of superoxide dismutase (SOD) with hydroxylamine, the activity of phosphorylated p38 MAPK with Western blot, the pathology with light microscope, and the extents of cell apoptosis were showed by the ratio of the apoptotic cells which had less DNA to the total cells of a cell-suspension sample by using the flow cytometry after being stained with propidium iodide. Results Compared with both control, CO inhalation and intraperitoneal infusion group at the same time point, the levels of PAF, ICAM-1, MDA, MPO, cell apoptosis rate and the phosphorylated p38 MAPK protein in LPS group were increased, while IL-10 and SOD were decreased (P ＜ 0.05 or 0.01), and accompanied by severe intestinal tract injury. There were no statistics differences at the different time point in the same group. PAF, ICAM-1, MDA, MPO and cell apoptosis rate in both LPS+CO inhalation group and LPS+CO intraperitoneal infusion group were lower, while IL-10 and SOD were higher than the corresponding value in LPS group at the same time point (all P ＜ 0.05), with ameliorate injury too, but the expression of phosphorylated p38 MAPK was further up-regulated than that of LPS group (all P ＜ 0.05). However, there were no significant differences in these parameters between LPS+CO inhalation group and LPS+CO intraperitoneal infusion group. Conclusion 250 ml/m3 CO inhalation and intraperitoneal infusion exerts the similar protection against LPS induced rat intestinal tract injury via anti-oxidant, anti-inflammation, and anti-apoptosis. This may involve the p38 MAPK pathway.
OBJECTIVE: To observe the changes of heme oxygenase-1 (HO-1) expression in the skeletal muscle after ischemia-reperfusion of hind limb in rats. METHODS: A model of hind limb ischemia was made by clamping femoral artery with a microvascular clip. Soleus muscle was obtained from the animals received sham operation, 4 h ischemia without reperfusion and 2 h, 4 h, 8 h, 16 h, 24 h reperfusion after 4 h ischemia. Soleus histology and malondialdehyde (MDA) content were measured. The levels of HO-1 mRNA and protein were measured in different time by Northern blotting, Western blotting and immunohistochemistry technique. RESULTS: After ischemia-reperfusion of limb, HO-1 mRNA increased at the 2nd hour, reached a peak at the 8th hour, and returned toward baseline at the 24th hour. The change of protein level was essentially in agreement with that of mRNA. Immunohistochemical results showed that HO-1 expressed primarily in skeletal muscle cytoplasma. There were no positive signals of mRNA and protein in sham group and in ischemia group. After limb reperfusion, MDA contents in the soleus muscle increased significantly when compared with that in the sham group (P lt; 0.05). MDA content of the 8th after reperfusion decreased significantly when compared with that of the 4 h after reperfusion (P lt; 0.05). CONCLUSION: Ischemia-reperfusion can induce HO-1 expression in skeletal muscle in rats, which may provide protection for injured tissue.
摘要:目的: 在风湿性心脏病患者瓣膜置换术中,评价罗库溴铵在麻醉诱导期间对患者心肌氧供和氧耗平衡的影响。 方法 :选择86例在中低温体循环下行瓣膜置换术的患者,采用随机双盲法分配成罗库溴铵组(n=42例)和维库溴铵组(n=41例)。给予咪唑安定(005～01 mg/kg)及芬太尼(10～15μg/kg)及等效剂量的罗库溴铵06 mg/kg或维库溴铵01 mg/kg(Org. Comp)进行麻醉诱导。监测麻醉诱导前至插管后10分钟(1次/1分)期间两组患者心肌氧供和氧耗的变化。 结果 :与基础值相比,罗库溴铵组患者在插管后5分钟期间心率增加了174%～135%,动脉收缩压增加了1694%～143%,平均动脉压增加了151%～132%。同期心率收缩压乘积增加了2267%～1396% (〖WTBX〗P lt;005)。心率和动脉血压在插管后1～7分钟期间明显高于同期的维库溴铵组患者(〖WTBX〗P lt;005)。 结论 :在ASA ⅢⅣ级、心功ⅡⅢ级风心病瓣膜病变患者进行瓣膜置换术中, 06 mg/kg罗库溴铵有潜在增加患者心肌耗氧量的作用。Abstract: Objective: To evaluate the effects of rocuronium on myocardial oxygen supplydemand in patients with rheumatic heart disease (RHD) during induction. Methods : 86 patients of either sex (ASA status ⅢⅣ; New York Heart Association classes ⅡⅢ) scheduled for valve replacement surgery were included in this randomized clinical trial (RCT). SwanGanz catheter was placed via right internal jugular vein before the induction of anaesthesia. Anaesthesia was induced with midazolam 00501mg.kg-1 and fentanyl 1015 μg·kg-1. The patients were randomized to receive either rocuronium 06 mg·kg-1 (group R, 〖WTBX〗n= 42) or vecuronium 01 mg·kg-1 (group V, 〖WTBX〗n= 41) to facilitate tracheal intubation when bispectral index (BIS) value dropped to 60 All data were recorded at the time before anaesthesia (Tb), loss of consciousness (Ts), administration of muscle relaxant (Tm), 1 min after administration of muscle relaxant (T1), when trainoffour stimulation (TOF) reached 0 (T2) and 1,2,3,4,5,7,10 min after tracheal intubation (T39).〖WTHZ〗Results : Heart rate (HR) increased by 174%135%, systemic arterial systolic pressure (SAP) increased by 1694%143%, mean arterial systolic pressure (MAP) increased by 151%132% and product of heart rate and arterial systolic pressure(RPP) increased 2267%1396% respectively during 5 minutes after intubation as compared with baseline in group R, which were significantly higher than those in group V during 5 minutes after intubation (〖WTBX〗P lt;005). Conclusion : An intubation dose of rocuronium should be used cautiously in patients with rheumatic heart disease (ASA status ⅢⅣ; NYHA classes IIⅢ).
We assayed the levels of free radical and scavenger in the blood and lens of streptozotocin-in-duced diabetic SD rats, and found that the levels of lipoperoxide(LPO),MDA were higher than that of normal SD rats, and the total superoxygen dismutase (T-SOD), Cu-Zn-SOD) were lower that that of normal rats ( P lt;0.01 ). Simultaneous injection of streptozotocin and large dose of SOD could no avoid the occurence of diabetes mllitus, but did improve the metabolism of free radical in blood and lens. Hence, we think that large dose of SOD might be effective in preventing to development of diabetic cataract which is related to deterioration of free radical metabolism. （Chin J Ocul Fundus Dis,1994,10:25-27）
短期进入高原从事高强度工作所致高原反应是值得探讨的问题,查阅文献,探讨其病因及发病机理、临床表现,总结国内外在诊断、预防及治疗方面的经验,探索一套可行、有效的预防及治疗措施,具有重要的临床意义。
【摘要】 目的 观察长期大量酒精摄入对大鼠心肌结构及心肌组织中丙二醛(MDA)、超氧化物歧化酶(SOD)和金属硫蛋白(MT)含量的影响,探讨氧化应激在酒精性心肌病大鼠中的作用。 方法 雄性健康SD大鼠45只,随机分为2组,即对照组20只和模型组25只。模型组酒精浓度从5%、10%、20%和30%依次各自由饮1周,然后递增至36%后以该浓度维持饲喂。对照组每日饮用与模型组酒精同等热量的葡萄糖水。6个月后,观察大鼠心肌组织的形态学改变及超微结构的变化,测定心肌组织中MDA、SOD及MT的含量。结果 模型组大鼠心肌细胞排列紊乱、间质充血、炎细胞浸润、线粒体肿胀、空泡形成、肌丝溶解、核膜不规则和核仁裂解。心肌组织中MDA含量明显升高(Plt;0.01),SOD活力含量明显降低(Plt;0.01),MT含量明显降低(Plt;0.01)。 结论 长期摄入大量酒精可使氧自由基代谢失衡,导致心肌损伤。氧化应激在酒精性心肌病发病机制中发挥着重要的作用。【Abstract】 Objective To observe the effect of longterm and large quantities of alcohol intake on myocardial structure of rats and the content of malondialdehyde (MDA), superoxide dismutase (SOD) and metallothionein (MT) in myocardium tissue. To study the effect of oxidative stress on the rats with alcoholic cardiomyopathy. Methods Fortyfive male and healthy SD rats were randomly divided into the control group (20 rats) and model group (25 rats).The alcoholic concentrate in model group was increased from 5%,10%,20% to 30% every week, and maintain free drinking mass concentration of 36% alcohol. The control group drink the same calories of glucose water. Six months later, the myocardial tissues were observed both in light microscope and electron microscope .The level of MDA、SOD and MT were tested in myocardium tissue. Results In the model rats, the cells of myocardial disarray, interstitial congestion, inflammatory cell infiltration, mitochondrial swelling, vacuole formation, melt filaments, irregular nuclear membrane and nucleolus cracking. The content of MDA incresed(Plt;0.01)and the activities of SOD decreased(Plt;001),levels of MT decreased (Plt;0.01) in the cardiac muscular tissues in the model group compared with the control group. Conclusion Longterm intake of large amounts of alcohol can break the balance of oxygen free radicals, which leading to the damage of myocardial. Oxidative stress plays an important role in the etiopathogenesis of alcoholic cardiomyopathy.
目的:寻找对腺病毒灭活的有效方法,来预防大规模生产腺病毒时所致的生产细胞的污染。方法:采用紫外线照射和不同浓度过氧乙酸的灭活方法灭活腺病毒,并将处理后的病毒加入到正常人胚肾293细胞中培养,观察细胞是否出现病变作为灭活效果判断标准。结果:我们发现一定强度紫外线照射至少2 h以上才能完全灭活腺病毒,过氧乙酸达到1 %的浓度和至少作用30 min,才能将完全病毒灭活。结论:紫外线照射2 h以上能有效灭活腺病毒,我们可以用于操作台的腺病毒灭活;1%浓度的过氧乙酸作用30 min以上能有效将腺病毒灭活,我们可以运用于实验室大空间的腺病毒灭活。
Objective The effects of endotoxin, cytokines, nitric oxide were reviewed in the development of hyperdynamic circulatory syndrome in portal hypertension. Methods Liceratures of overseas main studies in hyperdynamic circulatory syndrome of portal hypertension in recent 10 years were reviewed. Results The hyperdynamic circulatory syndrome was found in 30%-50% of patients with cirrhosis and in all animal models of portal hypertension. The research results of the effects of endotoxin, cytokines, nitric oxide in the development of hyperdynamic circulatory syndrome were different. Conclusion Hyperdynamic circulatory syndrome contribute to the maintenance and aggregation of portal hypertension. Endotoxin, cytokines, nitric oxide may play a role in the development of hyperdynamic circulatory syndrome. Nitric oxide is a more important factor. The effect of other factors is probably mediated by nitric oxide.