Effects of Ginsenosides and Ketoprofen on Smoke Inhalation Injury in Rabbits and Rats

Six hours after smoke inhalation injury in rabbits, the permeability of pulmonary vesselsand the aggregation of circulating platelets increased markedly accompanied with apparent patholog-ical changes in the trachea and lungs. Fifteen minutes after smoke inhalation injury in rabbits, an intravenous dose of ginsenosides or ketoprofenwas given to the animals respectively. 6 hours after medication, it was found that both the drugscould significantly alleviate the platelet aggregation, but only ginsenosides could alleviate theaugmentation of pulmonary vascular permeability and the pathological lesions in the trachea andlungs. In those rats injured by smoke inhalation, l hour after an intravenous dose of ginsenosides, theplasma PGI_2 level was elevated and TXA_2/PGI_2 ratio decreased significantly.     

人参皂甙和酮布芬对烟雾吸入性肺损伤的影响

家兔烟雾吸入伤后6h,肺血管通透性和循环中血小板聚集率均明显增加,气管和肺部也有明显病变。治疗组于伤后15min静注人参总皂甙或酮布芬后6h,虽然两种药物均使循环中血小板聚集率显著降低,但只有人参总皂甙能明显降低伤后增加的肺血管通透性和减轻气管和肺部的病变。大白鼠在类似的实验条件下,人参总皂甙给药后1h,可使血中PGI_2水平升高,TXA_2/PGI_2的比值明显下降。     

双丁酰cAMP对大鼠烟雾吸入性肺损伤的防治作用

目的：探讨细胞内第二信使分子cAMP稳定的人工合成同系物双丁酰cAMP对大鼠烟雾吸入性肺损伤的防治作用。方法：分别采用干湿重法、伊文思兰荧光法,放射免疫分析法,过氧化氢还原法、TBA色法测定肺组织含水量、肺微血管通透性（PMVP）、肺组织cAMP水平、髓过氧化物酶（MPO）活性及脂质过氧化物MDA含量。结果：大鼠吸入烟雾损伤后2hPMVP明显增大,6h达高峰;同时肺含水量、MPO活性及MDA含量显著升高,并出现呼吸衰竭的临床表现。与此相对应,肺组织cAMP水平进行性下降,在时相上与PMVP呈反相变化。双丁酰cAMP（Db-cAMP）于伤后立即ip能显著降低PMVP、肺含水量,减少肺组织的白细胞浸润,减轻脂质过氧化损害,且呈剂量依赖性;能升高细胞内cAMP的药物异丙肾上腺素（Iso）于伤后立即ip,也具有类似作用。结论：Db-cAMP对大鼠烟雾吸入性肺损伤具有防治作用,其机制与其减少肺组织白细胞浸润、减轻脂质过氧化损伤及降低吸入烟雾损伤大鼠PMVP有关。     

自由基在卡那霉素内耳中毒中的作用

探讨自由基在卡那霉素（ＫＭ）内耳中毒中的作用，方法：豚鼠６６只，分正常对照组，ＫＭ组，ＫＭ＋尼莫地平（ＮＤ）组，ＫＭ＋超氧化物歧化酶（ＳＯＤ）组，连续用药１２ｄ，停药４ｄ后，分别测试听性脑干反应（ＡＢＲ）阈移，血清ＳＯＤ和耳蜗组织丙二醛（ＭＤＡ），同时也对耳蜗组织作扫描电镜观察，结果：ＫＭ组ＡＢＲ阈移和耳蜗ＭＤＡ显著高于对照组，ＮＤ和ＳＯＤ组（Ｐ〈０．０１），其血清ＳＯＤ明显低于对照组（Ｐ〈０．０     

人参总皂甙对大鼠烟雾吸入性肺损伤的疗效与其抗氧化作用的关系

本实验采用大鼠烟雾吸入性肺损伤模型,观察了致伤后立即腹腔注射人参总皂甙(GS)对该损伤的作用。发现GS可明显减轻烟雾吸入所致PMVP增加,减少BALF中WBC计数和蛋白含量,使肺内WBC浸润,肺水肿,肺充血、出血等病变减轻。GS还可抑制致伤大鼠肺和血清MDA的升高,使已降低了的肺SOD活性恢复至正常水平以上。体外实验也发现,GS可有效地抑制肺匀浆过氧化脂质生成和清除O_2~-·、OH·。提示GS的治疗效果与其抗氧化作用有关。     

TRH对大鼠脊髓损伤脂质过氧化的影响

本实验以大鼠脊髓损伤(SCI,50gcm)模型,研究TRH对SCI脂质过氧化的影响。结果表明,于SCI后立即iv不同剂量的TRH(0.2mg/kg,0.6mg/kg,2.0mg/kg,每小时1次,连续4次),可显著地抑制伤段脊髓组织脂质过氧化反应,使丙二醛(MDA)含量显著降低,并呈剂量依赖关系j;TRH还可使组织超氧化物歧化酶(SOD)活性明显升高。提示TRH抗SCI脂质过氧化反应是通过升高SOD活性,清除自由基(尤其是氧自由基)介导的,它可能是1种有效的自由基清除剂。     

葛根素对异丙肾上腺素诱导大鼠心肌损伤的保护作用

采用异丙肾上腺素造成大鼠急性心肌缺血模型 ,观察葛根素对大鼠心电图、血清磷酸肌酸激酶 (CPK)、心肌组织超氧化物歧化酶 (SOD)和脂质过氧化物丙二醛 (MDA)的影响。发现葛根素可对抗异丙肾上腺素所致心肌缺血大鼠的心电图ST段的异常升高 ,使血清CPK降低 ,并可增加心肌组织SOD的活力 ,减少MDA生成。提示 :葛根素对大鼠心肌缺血有保护作用     

黄芩甙对异丙肾上腺素诱导大鼠心肌损伤的保护作用

利用异丙肾上腺素造成大鼠急性心肌缺血模型,观察黄芩甙对大鼠缺血心肌的保护作用。２８只Ｗｉｓｔａｒ大鼠分为正常对照组、缺血模型组、黄芩甙Ⅰ组、黄芩甙Ⅱ组。观察黄芩甙对各组大鼠心电图、血清磷酸肌酸激酶及心肌组织超氧化物歧化酶（ＳＯＤ）和脂质过氧化物丙二醛（ＭＤＡ）的影响。结果表明,黄芩甙可对抗异丙肾上腺素所致大鼠急性心肌损伤,使心肌缺血大鼠的心电图Ｓ Ｔ段异常抬高数减少,血清磷酸肌酸激酶（ＣＰＫ）降低,并可增加心肌组织ＳＯＤ的活力,减少ＭＤＡ生成。提示黄芩甙对大鼠心肌缺血有保护作用,其机制可能与抗脂质过氧化反应有关。     

大鼠视网膜光损伤MDA含量和形态学改变及SOD的治疗作用

目的 建立大鼠视网膜光损伤模型.检测视网膜光损伤时丙二醛（MDA）含量的变化和光镜改变,以及超氧化物岐化酶（SOD）的治疗作用.方法用自制光损伤装置建立大鼠视网膜光损伤模型,测定光损伤时不同时间点的MDA含量变化及光镜改变.结果大鼠视网膜光损伤时MDA含量增高,光镜下可见视网膜结构改变.结论SOD对大鼠视网膜光损伤有治疗作用,其机制是通过抗脂质过氧化作用.     

人参总皂甙对大鼠肾缺血再灌注损伤的保护作用

目的：观察研究人参总皂甙（GS）对肾缺血再灌注损伤的保护作用。方法：采用SD大鼠右侧肾切除，左侧肾蒂夹闭60min肾缺血后再灌注模型。将SD大鼠随机分组，除正常对照组外，分别注射生理盐水及人参总皂甙（GS）预防性用药。结果：GS组能明显抑,制缺血再灌注所致的血及肾组织脂质过氧化代谢产物丙二醛（MDA）的升高以及超氧化物歧化酶（SOD）活性的降低，肾病理学损害及超微结构改变明显改善。结论GS对肾缺血再灌注损伤具保护作用，可能主要是通过抗脂过氧休作用，保护抗氧化酶活性，清除氧自由基（OFR）而实现的。     

Ⅰ射线及烧伤复合伤对鼠肝LPO作用和相关酶活性的影响

本文观察了γ射线及烧伤复合伤后1 d～10d内大鼠肝线粒体MDA含量、细胞色素氧化酶、NADH-细胞色素C还原酶、CAT和SOD活力的动态变化,以反映肝线粒体内氧自由基、MDA产生和抗氧化机制的变化。结果表明线粒体MDA含量在烧伤、γ射线损伤和放烧复合伤后第2天、6天明显升高,其中烧伤组第10天有第3次高峰出现。细胞色素氧化酶和NADH-细胞色素C还原酶活力在3种损伤后有明显上升,而CAT和SOD活力在3种损伤后有明显下降。γ射线、烧伤及复合伤造成线粒体内产生O·_2~-和H_2O_2的酶活力增加,同时伴有清除O·_2~-和H_2O_2的CAT和SOD酶活力下降,这是造成线粒体膜脂质过氧化作用加速的原因之一。     

缺锌对血清、肝脏脂质过氧化的影响

本文研究缺锌对超氧化物歧化酶及脂质过氧化物的影响。缺锌组血和肝的LPO高于对照组,而SOD低于对照组;血VitE及CAT低于对照组。血LPO与锌,CAT、VitE呈负相关趋势。结果提示,严重缺锌时Cu-Zn-SOD合成减少。SOD能催化超氧化物自由基转化为过氧化氢,后者又为体内的CAT和GSH-PX所清除。     

别嘌呤醇对大鼠吸入性肺损伤的作用及其机制探讨

本实验采用大鼠烟雾吸入模型,观察了预先给予别嘌呤醇对吸入性肺损伤后6h内肺微血管通透性、丙二醛生成、超氧化物歧化酶活性、肺灌洗液中蛋白浓度及白细胞计数和血清丙二醛的影响,并辅以肺脏病理检查。结果表明:别嘌呤醇对吸入伤大鼠可以显著降低肺微血管通透性,减少肺灌洗液中蛋白含量及白细胞计数,组织病理学检查也可见肺充血、出血、间质和肺泡水肿减轻,白细胞浸润减少等。别嘌呤醇在减轻肺水肿的同时,也使肺及血清丙二醛水平明显降低,而肺组织丙二醛含量的变化在伤后6h内与肺微血管通透性、肺灌洗液中蛋白含量及白细胞计数的变化在时间及程度上都一致。以上结果提示,别嘌呤醇通过抑制黄嘌呤氧化酶,减少超氧阴离子产生,从而抑制肺脂质过氧化,减轻吸入性肺损伤。     

Respiratory Abnormalities Following Smoke Inhalation Injury in the Sheep

An arumal model to study smoke inhalation injuries was established in the sheep.22adult mate sheep were forced to inhale saw-dust smoke of pine wood for 6 minutes through anendotracheal tube.Pulmonury compliance,arterial blood gases,carboxyhemoglobin,andoxyhemoglobin were monitored and the morpholgical chanhes of the tracheobronchial tree andpulmonary parenchyma were studied with optical and eletron microscopy.Severe carbon monoxide poisorung with fatal blooa level of carboxyhemoglobin(higher than50％) was found at the end of smoie inhalation.Acute respiratory distress,progressivehypoxerrua decreased pulmonary compliance and increased P(A-α)O_2 and Q_s/Q_T oecurred af-ter the injury.Tracheobronchial blockage due to pseudomembranous cast,pulmonary edema,atelectasis,and necrosis of pulmonary epithelium were demonstrated on histological sections.The mechaniisms of carbon monoxide poisoning ane acute respiratory failure was discussed.     

Changes of Thromboxane and Prostacyclin after Smoke Inhalation Injury in Goats

Thirteen goats with chronic lung lymph fistula were inflicted withsmoke inhalation injury.Thromboxane A_2(TXA_2 in terms of thromboxane B_2 orTXB_2)and prostacyclin(PGl_2 in terms of 6-keto-prostaglandin F_(1x)or6-keto-PGF_1x)in plasma,lung lymph and lung tissue were measured withradioimmunoassay(RIA).Extravascular lung water(EVLW),lung lymph flow(QL),the ratio of protein contents between lung lymph and plasma(LIP),hemodynamic parameters,blood gases,platelet and leukocyte counts were alsodetermined.EVLW,QL and L/P increased significantly at the 1st hour,reachedtheir peak values at the 2nd hour,then declined gradually and remained at a levelover the baseline at the 6th hour after injury.TXA_2 and PGl_2 also increasedmarkedly and the.changes of TXA_2 and TXA_2/PGI_2 ratio were in parallel withthose of EVLW,QL and LIP both in degree and in length of time.It is possiblethat the increased TXA_2 and TXA_2/PGI_2 ratio might participate in the formationof permeability pulmonary edema through direct injury and for chemical mediatorsreleased by platelet and leukocyte aggregations promoted by TXA_2.In addition,TXA_2 might also play a role in the early elevation of pulmonary arterial pressure.     

Role of Lipid Peroxidation in Bacterial Translocation from the Small Intestine after Thermal Injury in Rats

Oxygen-derived free radicals have bran proved to play a role in the intestinalmucosa damage induced by ischemic reperfusion after burns,but their role in thebacterial translocation from the intestine to other organs is not documented so far.Theauthors intended to investigate this problem on 186rats,which were randomized into 5groups:the normal control group,the group receiving oral Pseudomonas,the group ofsimple burn injury,and the groups of combined oral Pseudomonas and burn injury withor without superoxide dismutase(SOD)treatment.The burn injury was 30% TBSA fullthickness scalding.The oral administered Pseudomonas was labdled with isothiocyanatefor tracing.The animals were killed in the 4th,12th,24th,48th,or 72nd hour afterinjury respectively.The changes of malondialdehyde(MDA)in the ilcal mucosa were ob-served with optical and electron microscope,and bacterial translocation from the intes-tine to the liver and blood stream was traced .The animals with combined injury and simple burns showed a marked increase ofileal mucosal MDA with the peak in the 12th hour accompanied with intense pathologicalchanges in the small intestine;the incidence of bacterial translocation from the intestineto other organs also increased.With SOD treatment,the MDA levd in the ileal mucosawas significantly lower,the pathological changes in the intestinal mucosa were allevia-ted,and the incidence of bacterial translocation from the intestine was lowered with nolabdled Pseudomonas isolated from the blood stream.In this study,it was demonstrated that free radicals are one of the factors ofintestinal mucosal damage and bacterial translocation from the intestine after burns,andSOD could protect the intestinal mucosal barrier from being injured and inhibit thebacterial translocation from the intestine.     

大鼠脑缺血再灌流损伤在脑震荡脑损伤中作用的研究

本实验采用单摆式打击装置建立大鼠脑震荡模型。病理组织学改变为伤后１５分钟开始出现全脑血管痉挛，３０分钟血管痉挛缓解，进入持续性充血状态，相继出现神经细胞退变和部分轴索肿胀、断裂。测定了脑皮质中ＬＰＯ含量呈明显时序性改变，伤后３０ｍｉｎ开始上升（Ｐ＜０．０５）。６０ｍｉｎ达高峰。证明了脑震荡脑损伤的形成是在暴力直接作用所致损伤的基础上，伴以缺血再灌流损伤。     

山羊烟雾吸入伤后早期肺损伤与活性氧变化的关系

本文通过慢性肺淋巴瘘,动态观察了清醒山羊(N=15)严重烟雾吸入伤后早期肺损伤与活性氧变化的关系。实验观察6h。检测SOD活性作为反映O_2~-的变化;EVLW、QL、L/P等作为反映肺损伤的指标。 实验结果表明,伤后均较早出现严重低氧血症、代谢性酸中毒合并呼吸性碱中毒,EVLW及QL伤后1h即明显增加,光镜下见肺间质和肺泡水肿。说明实验动物伤后出现了肺水肿和急性呼吸功能不全。在EVLW及QL增加的同时,CL、L/P及肺血管蛋白漏出量也增加,EVLW与L/P的变化密切相关。提示肺水肿主要系血管通透性增加所致。伤后肺淋巴液、动脉血活性氧变化比静脉血早,动脉血活性氧水平高于静脉血;肺组织、肺灌洗液活性氧及肺淋巴SOD清除重伤后均立即增加,表明吸入伤后活性氧立即增加,且主要来自肺部。活性氧的变化高峰与肺损伤程度的加重变化规律一致,且呈线性关系。提示活性氧可能参与了烟雾吸入伤后早期肺损伤、肺水肿发生和发展的作用。     

脂质过氧化在烟雾吸入性肺损伤机制中的作用

本文观察了脂质过氧化在犬(n=16)烟雾吸入性肺损伤机制中的作用。测定了动脉血SOD活性、动脉血浆MDA及呼出气乙烷和PaO_2及EVLW的变化。结果表明,本模型伤后早期出现了肺水肿和急性肺功能障碍。MDA及乙烷伤后显著增加,伤后30min及24h出现两峰值,SOD活性办增加。提示伤后早期氧自由基增加,肺脂质过氧化亢进。MDA及乙烷的第一个峰值与早期肺损伤及应激反应有关,第二个峰值与肺部感染有关。MDA、乙烷及SOD活性变化规律与PaO_2及EVLW相同。表明氧自由基导致的脂质过氧化可能参与了烟雾吸入伤后肺损伤发生和发展。     

依达拉奉对急性肺损伤的治疗作用及其机制探讨

目的探讨自由基清除剂依达拉奉对急性肺损伤大鼠模型的保护作用。方法将32只SD大鼠随机分为C组(生理盐水+生理盐水,n=8)、E组(生理盐水+依达拉奉,n=8)、LPS组(脂多糖+生理盐水,n=8)和LPS+E组(脂多糖+依达拉奉,n=8),各组经尾静脉注入LPS和依达拉奉或等体积生理盐水。6 h后麻醉大鼠并行动脉血气分析及肺病理学检查,检测血浆中肿瘤坏死因子α(TNF-α)和白介素6(IL-6)及肺组织中丙二醛(MDA)和NO水平。结果与C组相比,LPS组出现明显的肺损伤改变、动脉血氧分压显著下降[(99.37±4.35)mmHg vs(60.11±8.41)mmHg,P<0.01]、血浆中TNF-α[(3.89±0.53)pg/mL vs(11.95±1.97)pg/mL,P<0.01]和IL-6[(4.73±0.91)pg/mL vs(41.25±7.11)pg/mL,P<0.01]显著升高,肺组织中MDA[(2.06±0.42)nmol/mg vs(8.91±2.03)nmol/mg,P<0.01]和NO[(3.97±0.87)nmol/mg vs(8.74±2.01)nmol/mg,P<0.01]也显著升高;与LPS组相比,自由基清除剂依达拉奉使肺组织中MDA[(8.91±2.03)nmol/mg vs(3.76±0.68)nmol/mg,P<0.01]和NO[(8.74±2.01)nmol/mg vs(3.53±0.71)nmol/mg,P<0.01]显著降低,显著减轻急性肺损伤(ALI)大鼠的肺损伤程度,提高动脉血氧分压[(60.11±8.41)mmHg vs(85.69±6.41)mmHg,P<0.01],并使血浆中的TNF-α[(11.95±1.97)pg/mL vs(5.65±1.09)pg/mL,P<0.01]和IL-6[(41.25±7.11)pg/mL vs(11.06±1.27)pg/mL,P<0.01]显著降低。结论自由基清除剂依达拉奉能减轻急性肺损伤的病理生理变化,其机制在于依达拉奉能有效清除自由基并减少致炎因子的释放。