上呼吸道氨损伤的紧急医疗

因为装满液氨的液罐车和载客汽车相撞,液氨涌入客车内,有37名乘客遭受氨水和氨气损伤,主要是损伤面部皮肤、眼和上呼吸道.当时死于急性心衰1例,轻伤7例;

纤维支气管镜在救治氨气吸入性损伤患者中的应用

目的探讨纤维支气管镜(纤支镜,FOB)在氨吸入性损伤患者救治中的诊断及治疗价值。方法32例患者纤支镜检查全部在床旁或纤支镜室进行,同时进行心电图及无创脉氧测定监护,并对所有氨吸入性损伤患者临床和纤支镜检查资料进行回顾性分析。结果32例患者行纤维支气管镜检查78人次,其中床旁检查42人次,气管内吸痰与支气管灌洗36人次。3例行气管切开、并经纤维支气管镜急诊检查及治疗12人次。临床病例分型为:轻度10例,中度14例,重度8例。纤支镜下吸入性损伤分型为:轻度11例,中度9例,重度8例,特重度4例。全部病例救治成功,无严重并发症发生及病例死亡。结论纤维支气管镜在氨吸入性损伤患者救治中具有较大诊断及治疗价值,且有简单易行、安全有效、可视性强等优点,值得临床推广应用。

几种色素抑制过氧亚硝酸根损伤酪氨酸能力的对比

过氧亚硝酸根可以通过强氧化性及强硝化性损伤酪氨酸,从而损害人体健康.姜黄素、原花青素、槲皮素和柚皮素具有抗氧化、抗硝化性,但其自身颜色在研究酪氨酸硝化损伤的常规方法中易造成干扰.为测定色素抑制3-硝基酪氨酸生成的能力,使用高效液相色谱-二极管阵列检测器(HPLC-PDAD,High Performance Liquid Chromatography-Photodiode Array Detector)法对硝化损伤体系成分进行分离,使用荧光光谱法测定色素抑制酪氨酸二聚体生成能力,邻苯三酚自氧化法测定超氧根阴离子抑制能力.结果表明3-硝基酪氨酸抑制率从大到小为姜黄素、原花青素、柚皮素、槲皮素、V_C;酪氨酸二聚体抑制率从大到小为原花青素、姜黄素、柚皮素、槲皮素、V_C;邻苯三酚自氧化抑制率从大到小为姜黄素、槲皮素、柚皮素、V_C,原花青素无明显影响.分析表明4种色素成分抗氧化、抗硝化能力与其结构密切相关.

白藜芦醇对同型半胱氨酸损伤的人脐静脉内皮细胞的作用

目的:探究同型半胱氨酸(Hcy)损伤中白藜芦醇对人脐静脉内皮细胞的作用效果。方法:研究中通过建立Hcy诱导内皮细胞损伤的人脐静脉内皮细胞模型,观察不同浓度下白藜芦醇对人脐静脉内皮细胞小凹蛋白(CAV1)、一氧化氮(NO)系统变化。结果:人脐静脉内皮细胞增殖活性当Hcy浓度增加时活性减弱,且48hHcy损伤组的个指标水平均低于24h组;与空白对照组比较,Hcy损伤组的eNOS蛋白及NO含量比其低,白藜芦醇(不同浓度)加入后,eNOS蛋白含量升高,各组eNOS蛋白水平含量均比Hcy损伤组高,且0.1μmol/L白藜芦醇组升高的幅度最大,NO含量方面,也呈现上升趋势,各组NO含量均明显比Hcy损伤组高,其中以0.1μmol/L、1.0μmol/L的白藜芦醇组的NO含量升高幅度最为明显,有统计学差异性(P<0.05),NO系统、mRNA(CAV1);mRNA(eNOS)表达量、mRNA(CAV1)表达量;eNOS蛋白、CAV1蛋白;上述指标之间均为负相关(P<0.05)。结论:白藜芦醇对同型半胱氨酸损伤的人脐静脉内皮细胞中的CAV1蛋白表达具有抑制作用,可以提高eNOS表达,从而促进NO释放。

修补剂对涤/氨面料强力损伤评价方法及应用

涤纶修补剂对涤/氨色疵布有很好的回修效果,但涤纶修补剂在回修涤/氨面料时会造成氨纶强力损伤。文章以修补剂处理后面料的伸长率来评价氨纶强力损伤程度,探讨了涤/氨坯布氨纶含量和面料尺寸对氨纶强力损伤程度的影响。研究结果表明,以30%氨纶含量和长宽比相对较高的涤/氨坯布作为评价面料,有利于氨纶强力损伤评价。涤/氨修补剂TF-216G不会造成涤/氨坯布中的氨纶损伤且对涤/氨色疵布有较好的回修效果,移染率高于市场竞品。

重组人促红细胞生成素对缺氧缺血新生鼠脑损伤学习记忆能力的保护

目的:观察重组人促红细胞生成素对缺氧缺血性脑损伤新生鼠海马CA1区半胱氨酸天冬氨酸蛋白酶3的影响及对学习、记忆能力的保护作用。方法:实验于2002/2003在南京医科大学儿科医学研究所完成。选用7d龄SD大鼠62只,随机分为缺氧缺血模型组(n=22),重组人促红细胞生成素治疗组(n=20)和假手术组(n=20)。缺氧缺血模型组和治疗组结扎左侧颈总动脉,并吸入体积分数0.08的O2。假手术组不结扎颈总动脉,不缺氧。①缺氧缺血模型组和假手术组缺氧前腹腔注射生理盐水,治疗组腹腔注射生理盐水稀释的重组人红细胞生成素(500U/mL),剂量均为0.01mL/g。观察模型组和治疗组大鼠在缺氧过程中的躁动和抽搐情况;记录缺氧后0,6,12,24h时间点两组大鼠发生抽搐情况(自发左旋、夹尾左旋及夹尾尖叫)只数。②缺氧24h后随机取缺氧缺血模型组9只,治疗组10只,假手术组9只,取脑组织,在海马及小脑部位进行冠状切片,免疫组织化学法检测各组海马CA1区活化的半胱氨酸天冬氨酸蛋白酶3的表达。③取缺氧缺血模型组,治疗组和假手术组各10只,模型组与假手术组再行腹腔注射生理盐水,治疗组注射重组人红细胞生成素,剂量均为0.01mL/g,48h各组再注射一次。利用跳台实验观察各组大鼠生后75d学习、记忆潜伏期和错误次数。结果:模型组动物在缺氧缺血模型制作过程中死亡3只,治疗组及假手术组动物无死亡,均进入结果分析。①行为学结果:治疗组缺氧后24h自发左旋、夹尾左旋、夹尾尖叫的发生率与模型组比较明显降低大鼠[(16.7%、50%、50%),(66.7%、83.3%、91.7%),P<0.05]。②缺氧缺血后大鼠脑组织内活化半胱氨酸天冬氨酸蛋白酶3阳性细胞明显增多,在海马、大脑皮质分布较为密集。模型组、治疗组、假手术组海马CA1区单位面积内阳性细胞数差异有显著性意义[(41.38±2.09),(22.63±3.17),(10.52±2.70)个/mm2,F=296.20,P<0.01]。模型组明显高于假手术组,治疗组较模型组明显减少,但仍高于假手术组,差异非常显著(q=21.28,P<0.01)。③跳台试验:模型组学习潜伏期与假手术组相比明显延长;错误次数明显增多;记忆潜伏期明显缩短;错误次数显著增加。而治疗组较模型组学习、记忆能力明显改善,表现为学习潜伏期明显缩短;错误次数明显减少;记忆潜伏期明显延长;错误次数显著减少。结论:缺氧缺血性脑损伤新生大鼠海马半胱氨酸天冬氨酸蛋白酶3活性显著增高,重组人红细胞生成素能抑制半胱氨酸天冬氨酸蛋白酶3激活,减轻对新生鼠缺氧缺血的脑损伤,改善动物学习、记忆能力。

清肝抑脂汤对慢性肝损伤保护作用的研究

目的探索清肝抑脂汤(QYT)抗慢性肝损伤的保护作用的影响。方法将小鼠随机分为空白对照组,模型组,阳性药物组,清肝抑脂汤高剂量组,清肝抑脂汤低剂量组。首先建立慢性肝损伤模型,除空白对照组外,其余各组小鼠分别腹腔注射10%CCl4溶液,0.1ml/10g,每周2次,共6周。在建模的同时,各组小鼠分别给予相应的药物治疗。末次给药后次日摘眼球取血,分离血清,检测小鼠血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)酶的活性;同时取肝脏,常规病理切片,观察肝组织病理学变化。结果肝组织病理切片显示清肝抑脂汤能改善肝损伤程度;清肝抑脂汤能显著降低小鼠血清ALT(P<0.05,P<0.01)和AST(P<0.05,P<0.01)酶活性。结论清肝抑脂汤能显著降低受试小鼠血清ALT,AST及ALP酶活性,清肝抑脂汤对CCl4所致小鼠慢性肝损伤具有明显的保护作用。

重楼对多发骨折—脂多糖两次打击模型大鼠的保护作用

目的:探讨重楼总皂苷(RPTS)对多发骨折—脂多糖两次打击模型大鼠的保护作用。方法:将70只Wistar大鼠随机分成3组,除空白对照组外,其余2组按多发骨折—脂多糖两次打击致脓毒症并急性肺损伤动物模型标准制模,制模后1小时,重楼干预组予重楼总皂苷(RPTS)灌胃。干预后6小时,部分动物采血,以ELISA法检测血清中TNF-α、IL-1β及IL-6浓度;各组留取肺组织,光镜下进行病理形态观察。剩余动物用以观察死亡率。结果:重楼干预组大鼠血清TNF-α、IL-1β及IL-6浓度显著低于模型对照组(P<0.001)。死亡率,重楼干预组显著低于模型对照组(P<0.05)。结论:重楼总皂苷对多发骨折-脂多糖两次打击模型大鼠具有保护作用,机制可能与下调血清中的TNF-α、ΙΛ-1β、IL-6水平从而减轻炎症反应以及减轻急性肺损伤有关。

探析甲状腺激素测定在肝病患者中的临床价值

目的检测血清中甲状腺激素水平在慢性乙型肝炎、乙肝肝硬化患者中的变化,探究其临床价值。方法选取医院2016年1月—2019年12月收治的健康体检者48例、慢性乙型肝炎60例(轻、中、重患者各20例)、乙肝肝硬化患者60例(Child-Pugh A、B、C三组各20例),检测其血清促甲状腺激素(TSH)、四碘甲腺原氨酸(T4)、三碘甲腺原氨酸(T3)、游离四碘甲腺原氨酸(FT4)、游离三碘甲腺原氨酸(FT3),将结果进行比对;并将慢性乙型肝炎轻中重度患者及肝硬化患者中不同Child分级,进行对比及统计分析。结果慢性肝炎、肝硬化组患者TSH水平高于健康体检者,血清甲状腺素T3、FT3和T4、FT4的水平随肝功能损伤程度增加而降低,差异有统计学意义(P<0.05)。肝硬化组患者TSH水平随着肝功能级别升高而升高,但组间差异不具有统计学意义(P>0.05),血清T3、T4、FT3、FT4水平随着肝功能级别升高而降低,组间差异均有统计学意义(均P<0.05)。结论随着肝功能损伤程度增加,血清甲状腺激素T3、FT3和T4、FT4的水平逐渐降低。血清TSH会因肝功能损伤受影响,但无统计学意义。

Effect of atrial natriuretic peptide on ischemia-reperfusion injury in a porcine total hepatic vascular exclusion model

AIM： To evaluate the effect of ANP on warm I/R injury in a porcine THVE model.METHODS： Miniature pigs （mini-pigs） weighing 16-24 kg were observed for 120 min after reperfusion following 120 min of THVE. The animals were divided into two groups. ANP （0.1 μg/kg per min） was administered to the ANP group （n = 7）, and vehicle was administered to the control group （n = 7）. Either vehicle or ANP was intravenously administered from 30 min before the THVE to the end of the experiment. Arterial blood was collected to measure AST, LDH, and TNF-α. Hepatic tissue blood flow （HTBF） was also measured. Liver specimens were harvested for p38 MAPK analysis and histological study. Those results were compared between the two groups.RESULTS： The AST and LDH levels were lower in the ANP group than in the control group; the AST levels were significantly different between the two groups （60 min： 568.7 ± 113.3 vs 321.6 ± 60.1, P = 0.038 〈 0.05, 120 rain： 673.6± 148.2 vs 281.1±44.8, P = 0.004 〈 0.01）. No significant difference was observed in the TNF-α levels between the two groups. HTBF was higher in the ANP group, but the difference was not significant. A significantly higher level of phosphorylated p38 MAPK was observed in the ANP group compared to the control group （0min： 2.92± 1.1 vs 6.38 ±1.1,,P= 0.011 〈 0.05）.Histological tissue damage was milder in the ANP group than in the control group.CONCLUSION： Our results show that ANP has a protective role in I/R injury with p38 MAPK activation in a porcine THVE model.

N-acetylcysteine attenuates alcohol-induced oxidative stress in the rat

AIM: There is increasing evidence that alcohol-induced liverdamage may be associated with increased oxidative stress.We aimed to investigate free-radical scavenger effect of n-acetylcysteine in rats intragastrically fed with ethanol.METHODS: Twenty-four rats divided into three groups werefed with ethanol (6 g/kg/day, Group 1), ethanol and n-acetylcysteine (1 g/kg, Group 2), or isocaloric dextrose(control group, Group 3) for 4 weeks. Then animals weresacrificed under ether anesthesia, intracardiac blood andliver tissues were obtained. Measurements were performedboth in serum and in homogenized liver tissues.Malondialdehyde (MDA) level was measured by TBARSmethod. Glutathione peroxidase (GSH-Px) and superoxidedismutase (SOD) levels were studied by commercial kits.Kruskal-Wallis test was used for statistical analysis.RESULTS: ALT and AST in Group 1 (154 U/Land 302 U/L,respectively) were higher than those in Group 2 (94 U/L and155 U/L) and Group 3 (99 U/L and 168 U/L) (P＝0.001 forboth). Serum and tissue levels of MDA in Group 1 (1.84 nmol/mL and 96 nmol/100 mg-protein) were higher than Group 2(0.91 nmol/mL and 64 nmol/100 mg-protein) and Group 3(0.94 nmol/mL and 49 nmol/100 mg-protein) (P＜0.001 forboth). On the other hand, serum GSH-Px level in Group 1(8.21 U/g-Hb) was lower than Group 2 (16 U/g-Hb) andGroup 3 (16 U/g-Hb) (P＜0.001). Serum and liver tissue levelsof SOD in Group 1 (11 U/mL and 26 U/100 mg-protein)were lower than Group 2 (18 U/mL and 60 U/100 mg-protein)and Group 3 (20 U/mL and 60 U/100 mg-protein) (P＜0.001for both).CONCLUSION: This study demonstrated that ethanol-induced liver damage is associated with oxidative stress,and co-administration of n-acetylcysteine attenuates thisdamage effectively in rat model.

Glutamine is highly effective in preventing in vivo cobalt-induced oxidative stress in rat liver

AIM: To evaluate the in vivo effect of glutamine on cobaltgenerated oxidative stress and (HO-1) induction in rat liver.METHODS: Fasted female Wistar rats received a single injection of cobalt chloride (375 μmol/kg body weight) and then were killed at different times. Lipid peroxidation and soluble and enzymatic antioxidant defense system (reduced glutathione (GSH), catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD)) were measured in liver homogenates. Ferritin and ferritin iron contents as well as heme oxygenase-1 (HO-1) activity and expression were also determined. The antioxidant properties of glutamine (Gin) were also evaluated. RESULTS: Cobalt chloride increased lipid peroxidation (50% over control values) 1 h after treatment. GSH reached a minimum at 3 h (40%) increasing thereafter. Twelve hours after CoCl2 injection, the antioxidant enzymes CAT, GSH-Px and SOD also diminished by about 30%. Heme oxygenase-1 induction was observed 6 h after treatment reaching a maximum value of 14-fold over the controls, 12 h after cobalt treatment. A 1.7-fold increase in ferritin and ferritin-bound iron 24 h after treatment were also obtained. Administration of glutamine (300 mg/kg body weight) by gavage 24 h before CoCl2 treatment entirely prevented the increase in thiobarbituric acid reactive substances (TBARS) content, the decrease in GSH levels, and partially reverted heme oxygenase-1 induction. CONCLUSION: These results suggested that a natural product such as glutamine prevents glutathione depletion and consequently heme oxygenase induction.

Drug-induced liver injury in hospitalized patients with notably elevated alanine aminotransferase

AIM： To identify the proportion, causes and the nature of drug-induced liver injury （DILI） in patients with no- tably elevated alanine aminotransferase （ALT）. METHODS： All the inpatients with ALT levels above 10 times upper limit of normal range （ULN） were ret- rospectively identified from a computerized clinical laboratory database at our hospital covering a 12-mo period. Relevant clinical information was obtained from medical records. Alternative causes of ALT eleva- tions were examined for each patient, including bili- ary abnormality, viral hepatitis, hemodynamic injury, malignancy, DILI or undetermined and other causes. All suspected DILI cases were causality assessed usingthe Council for International Organizations of Medical Sciences scale, and only the cases classified as highly probable, probable, or possible were diagnosed as DILI. Comments related to the diagnosis of DILI in the medical record and in the discharge letter for each case were also examined to evaluate DILI detection by the treating doctors. RESULTS： A total of 129 cases with ALT 〉 i0 ULN were identified. Hemodynamic injury （n = 46, 35.7%）, DILl （n = 25, 19.4%） and malignancy （n = 21, 16.3%） were the top three causes of liver injury. Peak ALT val- ues were lower in DILI patients than in patients with hemodynamic injury （14.5 5.6 ULN vs 32.5 ：I： 30.7 ULN, P = 0.001）. Among DILI patients, one （4%） case was classified as definite, 19 （76%） cases were clas- sified as probable and 5 （20%） as possible according to the ClOMS scale. A hepatocellular pattern was ob- served in 23 （92%） cases and mixed in 2 （8%）. The extent of severity of liver injury was mild in 21 （84%） patients and moderate in 4 （16%）. Before discharge, 10 （40%） patients were recovered and the other 15 （60%） were improved. The improved patients tended to have a higher peak ALT （808 ＋ 348 U/L vs 623 ＋ 118 U/L, P = 0.016） and shorter treatment duration before discharge （8 ＋ 6 d vs 28 ~ 12 d, P = 0.008） compared with the recovered patients. Twenty-two drugs and 6 herbs were found associated with DILl. Antibacterials were the most common agents causing DILI in 8 （32%） cases, followed by glucocorticoids in 6 （24%） cases. Twenty-four （96%） cases received treatment of DILl with at least one adjunctive drug. Agents for treatment of DILI included anti-inflammatory drugs （e.g., glycyr- rhizinate）, antioxidants （e.g., glutathione, ademetionine 1,4-butanedisulfonate and tiopronin）, polyene phospha- tidyl choline and herbal extracts （e.g., protoporphyrin disodium and silymarin）. Diagnosis of DILl was not mentioned in the discharge letter in 60% of the cases. Relative to prevalent cases and cases from wards of internal medicine, incident cases and cases from surgi- cal wards had a higher risk of missed diagnosis in dis- charge letter [odds ratio （OR） 32.7, 95%CI （2.8-374.1）,CONCLUSION： DILI is mostly caused by use of anti- bacterials and glucocorticoids, and constitutes about one fifth of hospitalized patients with ALT 〉 10 ULN. DILI is underdiagnosed frequently.

Alanyl-glutamine dipeptide inhibits hepatic ischemiareperfusion injury in rats

AIM： To investigate the protective effect and mechanism of alanyl-glutamine dipeptide （Ala-GIn） against hepatic ischemia-reperfusion injury in rats. METHODS： Rats were divided into group C as normal control Group （/7=16） and group G as alanyl-glutamine pretreatment 07=16）. Rats were intravenously infused with 0.9% saline solution in group C and Ala-GIn -enriched （2% glutamine） 0.9% saline solution in group G via central venous catheter for three days. Then all rats underwent hepatic warm ischemia for 30 min followed by different periods of reperfusion. Changes in biochemical parameters, the content of glutathione （GSH） and the activity of superoxide dismutase （SOD） in liver tissue, Bcl-2 and Bax protein expression and morphological changes of liver tissue were compared between both groups. RESULTS： One hour after reperfusion, the levels of liver enzymes in group G were significantly lower than those in group C （P〈0.05）. Twenty-four hours after reperfusion, the levels of liver enzymes in both groups were markedly recovered and the levels of liver enzyme in group G were also significantly lower than those in group C （P〈0.01）. One and 24 h after reperfusion, GSH content in group G was significantly higher than that in group C （P 〈0.05）. There was no statistical difference in activities of SOD between the two groups. One and 24 h after reperfusion, the positive expression rate of Bcl-2 protein was higher in group G than in group C （P〈0.05） and the positive expression rate of Bax protein was lower in group G than in group C （P〈0.05）. Histological and ultrastructural changes of liver tissue were inhibited in group C compared to group G. CONCLUSION： Our results suggest that Ala-GIn pretreatment provides the rat liver with significant tolerance to warm ischemia-reperfusion injury, which may be mediated partially by enhancing GSH content and regulating the expression of Bcl-2 and Bax proteins in the liver tissue.

Interaction of L-Arginine-methyl ester and Sonic hedgehog in liver ischemia-reperfusion injury in the rats

AIM： To investigate the role of Sonic hedgehog （Shh） on the course of liver ischemia and reperfusion （I/R） in rats, and the interaction between treatment with nitric oxide donor L-Arginine-methyl ester （L-Arg） and up-regulation of Shh expression.METHODS： A total of 30 male Sprague-Dawley rats weighing 220-240 g were used in this study. Shamcontrol group （G1, n = 10）： a sham operation was performed （except for liver I/R）. I/R-untreated group （G2, n = 10）： rats underwent liver ischemia for 1 h followed by reperfusion for 45 min. I/R-L-Arg group （G3, n = 10）： after performing the same surgical procedure as in group 2, animals were treated with L-Arg. Liver tissues were taken for determination of malondialdehyde （MDA） levels, and biochemical and histological evaluations were made.RESULTS： Plasma alanine aminotransferase （ALT）, aspartate aminotransferase （AS-T）, lactate dehydrogenase （LDH） and T-glutamyltranspeptidase （GGT） activities were higher in group 2 than in group 3. MDA values and the hepatic injury score decreased in the L-Arg treated group compared to the I/R-untreated group. In group 2, the hepatoo/tes were swollen with marked vacuolization. Group 3 rats showed well-preserved liver parenchyma, with hepatocytes extending from the central vein. The morphology of the hepatocytes and the sinusoidal structures was normal, without any signs of congestion. Mild Shh positive immunostaining was detected in group 2 animals. The expression of immunoreactive cells was increased markedly in liver tissue from I/R-L-Arg rats.CONCLUSION： Our findings suggest that Shh molecules are critical factors in the pathophysiology of inflammatory liver injury induced by I/R. In addition, NO plays an important role in the immunohistochemical expression of these molecules.