参附注射液对兔移植肺缺血-再灌注损伤的保护作用

目的观察参附注射液对供肺缺血-再灌注损伤的保护作用。方法将20只新西兰白兔随机分为实验组和对照组,每组各10只,建立兔左肺自体原位移植模型,分别用参附注射液和生理盐水对兔肺进行预处理和供肺灌注。于主动脉阻断前、再灌注后15min、30min和60min各时点检测左肺静脉血中丙二醛(MDA)含量、总超氧化物歧化酶(SOD)的活力,于再灌注60min后称左肺组织的干湿比重(D/W),并观察其病理变化。结果主动脉阻断前两组MDA含量差异无统计学意义(P0.05);再灌注15min后实验组MDA含量较主动脉阻断前下降;再灌注30min和60min时,两组MDA含量均呈上升趋势,但实验组明显低于对照组(P0.05)。主动脉阻断前实验组SOD活力明显高于对照组(P0.05),再灌注后两组SOD活力均呈下降趋势,以对照组下降幅度明显(P0.05)。实验组的D/W显著高于对照组(0.23±0.01vs.0.19±0.02,P0.05)。对照组肺组织水肿明显,大量的炎性细胞浸润,肺泡腔内有片状渗出;而实验组表现为肺泡间隔水肿轻微,少量炎细胞浸润,渗出不明显。结论参附注射液对供肺的缺血-再灌注损伤有较好的保护作用。     

体外循环中白细胞对肺损伤机制及白细胞过渡的肺保护作用

肺损伤为体外循环术后常见的并发症之一，血液与体外循环管道接触，能够活化补体，激活白细胞，白细胞激活后黏附于血管内皮细胞或进入肺组织，释放具有趋化作用的炎性介质及代谢产物，如蛋白酶，氧自由基和花生四烯酸等在肺损伤中起着重要作用，动物实验及临床应用白细胞过滤器在体外循环中对白细胞进行过滤，肺血管阻力明显降低，血氧饱和度，动脉血氧分压升高，尤其对术前缺氧越重和体外循环时间越长的患者作用越明显，因此，在体外循环中进行白细胞过滤能够减轻其对肺的损伤，起到肺保护作用。     

人参皂甙Rb1对肺缺血再灌注损伤的保护作用

目的探讨人参皂甙Ｒｂ１对肺缺血再灌注损伤的保护作用。方法按肺移植供肺获取和保存的方法，对３５只家兔的肺分别获取，保存；然后采用体外装置，建立体外肺缺血再灌注损伤模型。在即将再灌流前，将不同剂量的Ｒｂ１加入到５０ｍｌ再灌流血液中。结果Ｒｂ１可使肺组织中超氧化物歧化酶（ＳＯＤ）含量升高，丙二醛（ＭＤＡ）含量降低；使肺动脉压（ＰＡＰ）降低，湿肺干肺比重降低和改善肺组织病理变化。Ｒｂ１在再灌流血液中浓度为８０ｍｇ／Ｌ时，已有明显效果。结论Ｒｂ１对肺缺血再灌注损伤具有明显的保护作用。     

Analgesic and Antiinflammatory Effects of Two Novel κ-Opioid Peptides

Background: This study investigates two new [kappa]-agonist tetrapeptides, FE 200665 and FE 200666, with high peripheral selectivity as a result of poor central nervous system penetration.

Methods: Four days after administration of Freund adjuvant into the hind paw of male Wistar rats, antinociceptive effects of intraplantar and subcutaneous injection of FE 200665 and FE 200666 were measured by paw pressure algesiometry and compared with the [kappa]-agonist U-69,593. Peripheral and [kappa]-receptor selectivity was assessed by the antagonists naloxone methiodide (NLXM) and nor-binaltorphimine, respectively. Antiinflammatory effects were evaluated by paw volume plethysmometry and histologic score.

Results: Similar to intraplantar U-69,593, intraplantar FE 200665 (3-100 [mu]g) and FE 200666 (1-30 [mu]g) resulted in significant and dose-related increases of paw pressure thresholds. Higher doses of FE 200665 (0.2-20 mg) and FE 200666 (0.06-6 mg) were required by subcutaneous route to produce similar antinociceptive responses, supporting a peripheral site of action. nor-Binaltorphimine dose-dependently antagonized this effect, implying [kappa]-opioid selectivity. Analgesic effects of subcutaneous FE 200665 and FE 200666 were abolished by intraplantar nor-binaltorphimine, and both subcutaneous and intraplantar effects were dose-dependently antagonized by subcutaneous NLXM, further demonstrating a peripheral site of action. One to 6 days after Freund adjuvant inoculation, single and repeated intraplantar injections of FE 200665, FE 200666, and U-69,593 significantly reduced paw volume and histologic scores. Both changes were reversed by intraplantar nor-binaltorphimine and subcutaneous NLXM.     

己酮可可碱在肺缺血-再灌注损伤中的作用

目的　探讨己酮可可碱 (PTX)对肺缺血 -再灌注损伤的保护作用。　方法　 72只大鼠随机分为 3组 ,每组 2 4只。 组 :未行缺血及再灌注处理 ; 组 :行左肺缺血和再灌注处理 ; 组 :行左肺缺血和再灌注处理 ,并给予己酮可可碱。采用在体肺温缺血 -再灌注损伤的模型 ,于缺血 45分钟、再灌注 1小时、2小时和 4小时进行动脉血气分析、肺组织含水量、支气管肺泡灌洗液白蛋白含量、血浆和左肺组织丙二醛、左肺组织和支气管肺泡灌洗液髓过氧化物酶(MPO)活性测定。　结果　 组再灌注 2小时和 4小时动脉血氧分压显著降低 ,各时间点左肺含水量、支气管肺泡灌洗液白蛋白含量、血浆丙二醛、左肺组织、支气管肺泡灌洗液中髓过氧化物酶均显著升高 ,PTX可改善上述指标变化。结论　 PTX通过抑制中性粒细胞肺内聚集 ,减轻肺血管内皮细胞损伤程度 ,而防止损伤的发展     

Histopathological and Biochemical Effects of Ecballium elaterium on Sepsis-Induced Lung Injury

Purpose: The aim of this study was to investigate the role of Ecballium elaterium (EE) on sepsis-induced lung injury. Materials and Methods: A total of 30 male rats were divided into three groups as follows: control, sepsis, and treatment groups (sepsis + EE) with each group containing 10 rats. A rat model of sepsis induced by cecal ligation and puncture (CLP) was used. In the treatment group, rats were injected intraperitoneally with 2.5 mg/kg EE after CLP. Interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) values after a 24-hr period were measured via cardiac puncture. Animals were harvested after the procedure and biochemical analysis was done and histopathological changes of the tissue sections of lungs were examined thereafter. Results: A statistically significant decrease was observed in the IL-6 (p < .05), TNF-α (p < .05), and TOS (p < .01) levels in the sera of the treatment group compared to those of the sepsis group. Following the treatment, the TOS (p = .01) and OSI (p < .05) levels in the lung tissue of rats indicated a statistically significant decrease compared to those of the sepsis group. The histopathological follow-up undertaken after the administration of the EE treatment to septic rats showed significantly lower values of alveolar wall thickness (p < .001), interstitial edema (p = .018), and neutrophil infiltration (p = .047). Conclusion: EE treatment may have beneficial effects on sepsis-induced lung injury, and therefore has potential for clinical use.     

间断肺通气对体外循环肺损伤的保护作用

目的研究间断肺通气对体外循环(CPB)肺损伤的保护作用,并探讨其机制。方法将24例风湿性心脏病患者采用随机数字表法分为两组,处理组(n=13)CPB期间每5min间断肺通气一次;对照组(n=11)CPB期间不通气。所有患者均在术前留取血液标本,术后2h行支气管肺泡灌洗,分别测定支气管肺泡灌洗液(BALF)中的中性粒细胞、总蛋白(TP)、肿瘤坏死因子-α(TNF-α)含量、血清总蛋白以及术前、CPB后1h、4h肺氧合指数(OI)。结果处理组BALF中的中性粒细胞、TP、TNF-α含量较对照组显著降低(P<0.01,P=0.02,0.02),CPB后OI较对照组显著降低(P<0.05);两组CPB后1h、4h其OI均较同组CPB前显著增高(P<0.05)。结论间断肺通气可通过减少白细胞与血管内皮的黏附,减轻肺部炎症反应、内皮细胞损伤等,对CPB所致的肺损伤有保护作用。     

The Protective Effects of Caffeic Acid Phenethyl Ester on Acetylsalicylic Acid-induced Lung Injury in Rats

Aim: We aimed to investigate the protective effect of caffeic acid phenethyl ester (CAPE) on acetylsalicylic acid (ASA)-induced lung damage in rats in the present study. Methods: A total of 40 rats were randomly divided into five groups, with eight rats in each group—group 1: control, not receiving any medication; group 2: ASA (50 mg/kg/day); group 3: ASA (50 mg/kg/day) plus CAPE (20 μg/kg/day); group 4: ASA (100 mg/kg/day); and group 5: ASA (100 mg/kg/day) plus CAPE (20 μg/kg/day). ASA and CAPE were given via orogastric gavage for 5 days. The total oxidant status (TOS), total antioxidant capacity (TAC), oxidant stress index (OSI), and paraoxonase-1 (PON-1) activity of the blood samples and lung tissues were determined. Histopathological examinations of the lung tissues were performed by using light microscopic methods. Results: CAPE treatment significantly increased antioxidant PON-1 level both in the lung tissue and plasma (p < .05). Plasma antioxidant marker (TAC, PON-1) levels significantly increased and oxidant marker (TOS, OSI) levels significantly decreased in CAPE-treated rats (groups 3,5) compared to ASA given no-CAPE groups (group 2,4) (p < .05). Treatment with CAPE improved pulmonary interstitial inflammation and eosinophil accumulation due to ASA histopathologically. Conclusion: Eosinophil-rich inflammation and oxidative stress play important roles in ASA-induced lung toxicity, and CAPE may protect against ASA-induced lung toxicity by reduction of oxidative damage and inflammation in rats.     

Protective Effects of Isoflurane Pretreatment in Endotoxin-induced Lung Injury

Background: The concept of antiinflammatory effects of volatile anesthetics is well established in vitro and in some organ systems. Their protective role in lung injury, however, remains to be elucidated. The authors hypothesized that in the lung, isoflurane pretreatment may attenuate neutrophil infiltration and reduce endotoxin-induced injury.

Methods: Male C57Bl/6 mice were exposed to aerosolized lipopolysaccharide. Neutrophil recruitment into the pulmonary vasculature and migration into the different lung compartments (interstitium and alveolar air space) were determined by flow cytometry. Capillary protein leakage, formation of lung edema, and concentration of the chemokines keratinocyte-derived chemokine (CXCL1) and macrophage inflammatory protein 2 (CXCL2/3) in bronchoalveolar lavage were compared in mice with or without isoflurane treatment (1.4% inspired for 30 min) at different times before and after endotoxin exposure.

Results: Endotoxin inhalation induced significant neutrophil migration into all lung compartments. Isoflurane pretreatment attenuated both neutrophil recruitment into lung interstitium and alveolar space when given 1 or 12 h before or 1 h after lipopolysaccharide but not at 4, 6, or 24 h before endotoxin exposure. Isoflurane pretreatment 1 or 12 h before lipopolysaccharide also reduced protein leakage and pulmonary edema. Production of CXCL1 and CXCL2/3 in the bronchoalveolar lavage was reduced when isoflurane was given 1 h but not 12 h before lipopolysaccharide, suggesting different mechanisms for early and late protection.     

依达拉奉对大鼠重症急性胰腺炎肺损伤的影响

目的探讨依达拉奉(edaravone)对大鼠重症急性胰腺炎(SAP)肺损伤的影响。方法36只成年SD大鼠随机分为正常对照组、模型组及依达拉奉组,每组12只,经胰胆管逆行注射5%牛磺胆酸钠建立SAP大鼠模型。依达拉奉组给予依达拉奉,正常对照组和模型组则给予等量生理盐水。术后6h处死大鼠,检测其血清和肺组织匀浆中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,血清中肿瘤坏死因子-α(TNF-α)及白介素(IL)-1、IL-6含量,并计算肺干/湿重比(D/W)。结果模型组血清及肺组织中MDA含量以及血清TNF-α、IL-1和IL-6水平均明显高于正常对照组及依达拉奉组(P0.05),依达拉奉组血清及肺组织中MDA含量以及血清TNF-α、IL-1和IL-6水平也明显高于正常对照组(P0.05);而模型组肺D/W、血清及肺组织中SOD活性则明显低于其他2组(P0.05)。结论依达拉奉能减轻大鼠SAP导致的肺损伤。     

Protective Effects of Alpha-Lipoic Acid on Methotrexate-Induced Oxidative Lung Injury in Rats

Objective: Oxidative stress is one of the major causes of methotrexate induced lung injury (MILI). Alpha-lipoic acid (ALA), which occurs naturally in human food, has antioxidative and anti-inflammatory activities. The aim of this study was to research the potential protective role of ALA on MILI in rats. Methods: Twenty one rats were randomly subdivided into three groups: control (group I), methotrexate (MTX) treated (group II), and MTX+ALA treated (group III). Lung injury was performed with a single dose of MTX (20 mg/kg) to groups 2 and 3. On the sixth day, animals in all groups were sacrificed by decapitation and lung tissue and blood samples were removed for histological examination and also measurement the levels of interleukin-1-beta (IL-1β), malondialdehyde (MDA), glutathione (GSH), tumour necrosis factor-alpha (TNF-α), myeloperoxidase (MPO), and sodium potassium-adenosine triphosphatase (Na+/K+ATPase). Results: In MTX group tissue GSH, Na+/K+ATPase activities were lower, tissue MDA, MPO and plasma IL-1?, TNF-? were significantly higher than the other groups. Histopathological examination showed that lung injury was less severe in group 2 according to group 3. Conclusions: Oxidative damage of MTX in rat lung is partially reduced when combined with ALA.     

Protective Effects of Nigella sativa Oil in Hyperoxia-Induced Lung Injury

BackgroundOxygen-induced lung injury is believed to lead to the development of bronchopulmonary dysplasia in premature infants. We have evaluated the beneficial effects of Nigella sativa oil (NSO) on rats with hyperoxia-induced lung injury.MethodsThirty newborn Sprague-Dawley rats were randomly divided into 3 groups as hyperoxia (95% O₂), hyperoxia+NSO and control (21% O₂). Pups in the hyperoxia+NSO group were administered intraperitoneal NSO at a dose of 4 ml/kg daily during the study period. Histopathologic, immunochemical, and biochemical evaluations (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], malonaldehyde [MDA] and myeloperoxidase [MPO]) were performed.ResultsIn the histopathologic and immunochemical evaluation, severity of lung damage was significantly lower in the hyperoxia+NOS group (P<.05). Tissue GSH-Px and SOD levels were significantly preserved, and MDA, MPO levels were significantly lower in the hyperoxia+NSO group (P<.05).ConclusionNSO significantly reduced the severity of lung damage due to hyperoxia.     

Effects of Neutrophil Elastase Inhibitor on Progression of Acute Lung Injury Following Esophagectomy

The purpose of this study was to evaluate the effect of sivelestat sodium hydrate, a selective inhibitor of neutrophil elastase in the systemic inflammatory response, pulmonary function, and the postoperative clinical course following esophagectomy. Patients with hypoxia associated with surgical stress in the intensive care unit (ICU) immediately after an esophagectomy were eligible for this study. The degree of hypoxia was calculated according to the ratio of arterial oxygen tension (PaO₂) to the fractional concentration of inspired oxygen (FiO₂)—PaO₂/FiO₂. Patients with PaO₂/FiO₂ < 300 mmHg were enrolled in this study. Seven patients were treated with sivelestat, and 10 were not so treated. The degree of hypoxia, the criteria for systemic inflammatory response syndrome (SIRS), and the postoperative clinical course were compared between the two groups. The postoperative decreases in the PaO₂/FiO₂ ratio were significantly suppressed in the sivelestat group (p < 0.05, by analysis of variance, or ANOVA). Furthermore, 9 of the 10 control group patients developed SIRS on postoperative day 2, whereas only 2 of 7 of the sivelestat group patients developed SIRS (p < 0.05). The postoperative increases in the heart rate were significantly suppressed in the sivelestat group (p < 0.05, ANOVA). The postoperative decreases in the platelet counts were significantly suppressed in the sivelestat group (p < 0.05, ANOVA). The duration of mechanical ventilation and the length of ICU stay for the sivelestat group were shorter than that for the control group. We demonstrated that the postoperative decreases in the PaO₂/FiO₂ ratio following esophagectomy were significantly suppressed in the sivelestat-treated group. This clinical study showed that a neutrophil elastase inhibitor may thus be a potentially useful drug for treating acute lung injury following esophagectomy.     

Matrix Metalloprotease Expressions in Both Reperfusion Lung Injury and Oleic Acid Lung Injury Models and the Protective Effects of Ilomastat

Objective

Our aim was to study the expressions of matrix metalloprotease 9 (MMP9) and the effects of the MMP inhibitor Ilomastat in both ischemia/reperfusion (I/R)- and oleic acid (OA)-induced lung injury models.

Materials and Methods

Real-time polymerase chain reactions and Western blots were used to assess mRNA and protein expressions of MMP9 in lung tissues after I/R or OA lung injury. Ischemia was induced by clamping one branch of the pulmonary artery for 60 minutes and then reperfusing for 120 minutes. In the OA model, lung injury was induced by intravenous infusion of OA (0.1 mL/kg) for 20 minutes and then observation for 6 hours. Lavage leukocyte concentration and wet/dry lung weight ratio were used to assess lung inflammation and injury. Blood samples were collected for assays of hydroxyl radicals and nitric oxide. The MMP inhibitor Ilomastat (100 μg/kg) was administered before I/R and OA infusion.

Results

mRNA and protein expressions of MMP9 were significantly increased in both lung injury models. Ilomastat decreased MMP9 mRNA and protein expressions but did not reach statistical significance. Blood concentrations of hydroxyl radicals and nitric oxide, wet/dry lung weight ratios, and lavage leukocyte concentrations were significantly higher in both experimental groups compared with the sham group (P < .001). Ilomastat significantly attenuated the extent of lung inflammation and injury induced by both I/R and OA.

Conclusion

MMP may play a critical role in the lung injury induced by I/R and OA infusion.     

Effects of Peak Inspiratory Flow on Development of Ventilator-induced Lung Injury in Rabbits

Background: A lung-protecting strategy is essential when ventilating acute lung injury/acute respiratory distress syndrome patients. Current emphasis is on limiting inspiratory pressure and volume. This study was designed to investigate the effect of peak inspiratory flow on lung injury.

Methods: Twenty-four rabbits were anesthetized, tracheostomized, ventilated with a Siemens Servo 300, and randomly assigned to three groups as follows: 1) the pressure regulated volume control group received pressure-regulated volume control mode with inspiratory time set at 20% of total cycle time, 2) the volume control with 20% inspiratory time group received volume-control mode with inspiratory time of 20% of total cycle time, and 3) the volume control with 50% inspiratory time group received volume-control mode with inspiratory time of 50% of total cycle time. Tidal volume was 30 ml/kg, respiratory rate was 20 breaths/min, and positive end-expiratory pressure was 0 cm H2O. After 6 h mechanical ventilation, the lungs were removed for histologic examination.

Results: When mechanical ventilation started, peak inspiratory flow was 28.8 +/- 1.4 l/min in the pressure regulated volume control group, 7.5 +/- 0.5 l/min in the volume control with 20% inspiratory time group, and 2.6 +/- 0.3 l/min in the volume control with 50% inspiratory time group. Plateau pressure did not differ significantly among the groups. Gradually during 6 h, Pao2 in the pressure regulated volume control group decreased from 688 +/- 39 to a significantly lower 304 +/- 199 mm Hg (P < 0.05) (mean +/- SD). The static compliance of the respiratory system for the pressure regulated volume control group also ended significantly lower after 6 h (P < 0.05). Wet to dry ratio for the pressure regulated volume control group was larger than for other groups (P < 0.05). Macroscopically and histologically, the lungs of the pressure regulated volume control group showed more injury than the other groups.     

预处理对脱水蔬菜色素保存的影响

用不同保色溶液对胡萝卜、青椒和菜豆进行预处理，得出了其干制品色素保存率的最佳预处理方案，并讨论了金属离子预处理对青椒和菜豆的保绿效果，以及硫化处理对胡萝卜的保色效果。     

开肺陷胸汤对大鼠胰源性肺损伤的防治效应

目的：在制备大鼠胰源性肺损伤动物模型基础上给予中药治疗，动态观察血氧分压及二氧化碳分压变化，并对肺脏进行病理学分析。方法：实验分为模型组及中药治疗组,72h后观察肺脏病理变化及不同时间血气分析。结果：治疗组肺脏病理改变明显减轻（P＜0．05）；治疗组72h血氧分压明显高于模型组（P＜0．01），血二氧化碳分压明显低于模型组（P＜0．01）。结论：在胰源性肺损伤发病过程中，血氧分压及二氧化碳分压的变化直接反应出肺损伤病理改变的严重程度，治疗组随着氧分压升高，二氧化碳分压降低，标志着肺脏病理改变明显减轻。     

急性颅脑损伤两种氧疗效果的分析及护理

对５３例急性颅脑损伤病人采用两种氧疗方法，即高频通气和常规鼻导管吸氧法行氧疗的疗铲观察及分析结果表明：ＨＦＶ组氧疗后３０ｍｉｎ ＰａＯ２，ＳａＯ２明显升高，其中６４．３％的酸中毒病人通过ＨＦＶ治疗，ＰＨ恢复正常。而常规组氧疗２４ｈ后ＰａＯ２和ＳａＯ３未能得到明显改善。     

银杏叶提取物对体外肺缺血再灌注损伤保护作用的实验观察

目的:探讨银杏叶提取物对体外肺缺血再灌注损伤的保护作用.方法:按肺移植供肺获取和保存方法,对30只家兔的肺进行获取、保存,然后采用体外循环装置,建立体外肺缺血再灌注损伤模型.分3组,分别在手术前30 min从耳背静脉注入生理盐水、PGE1、银杏叶提取物.结果:银杏叶提取物和PGE1均可使肺组织中超氧化物歧化酶(SOD)含量升高,丙二醛(MDA)含量降低;使肺动脉压(PAP)降低,肺组织湿干重比降低;降低肺组织中的凋亡细胞数和改善肺组织病理变化.银杏叶提取物组的上述指标均优于对照组和PGE1组.结论:银杏叶提取物对肺缺血再灌注损伤有显著的保护作用.