Effects of early bronchoalveolar lavage fluid collected from dogs with smoke inhalation injury on the lungs of rats

Objective: Whether early massive bronchoalveolar lavage can remove the harmful substances from the lungs injured with smoke inhalation remains uncertain. This study was designed to observe the effects of early massive bronchoalveolar lavage fluid (BALF) on the healthy lungs in rats. Methods: Mongrel dogs were inflicted with severe smoke inhalation injury. The injured lungs were lavaged with large amount of normal saline in the first hour after injury and the BALF was collected. The BALF was injected into the healthy lungs of 30 rats (group C) in the dosage of 5 ml/kg. The functions and pathological changes of the lungs were observed 24 h after perfusion with the BALF. The data were compared with those of 23 rats (group B) whose lungs were perfused with the BALF collected from normal dogs and those of 21 rats (group A) whose lungs were perfused with normal saline. Results: The mortality rate 24 h after lung perfusion was higher in group C than in groups A and B. The survivors of group C exhibited fluctuation of respiratory rate (RR), remarkable decrease of PaO 2, significantly higher content of lung water, decrease of total static pulmonary compliance and pulmonary expansion index, and increasse of inflammatory cytokines in the tissues of lungs. Only slight mechanic obstructive effect on the airway was observed in rats of group A and B. The pathological changes of the lungs of the rats in group C were similar to those of the dogs with actual smoke inhalation injury. Conclusion: Our findings indicate that the BALF collected from dogs with acute severe smoke inhalation injury in the early stage after injury injured the normal lungs of rats with the bioactive substances in the BALF. These findings show us that it is a valuable therapeutic procedure to apply massive bronchoalveolar fluid lavage in the early stage after inhalation injury.

Effects of bone marrow-derived mesenchymal stemcells engraftment on vascular endothelial cell growthfactor in lung tissue and plasma at early stage of smoke inhalation injury

BACKGROUND： This study was undertaken to determine the effect of mesenchymal stem cells （MSCs） engraftment on vascular endothelial cell growth factor （VEGF） in lung tissue, plasma and extravascular lung water at early stage of smoke inhalation injury.METHODS： A rabbit smoke inhalation injury model was established using a home-made smoke inhalation injury generator, and rabbits were divided into two groups randomly： a control group （S group, n=32） and a MSCs treatment group （M group, n=32）. 10 ml PBS was injected via the ear marginal vein immediately at injury into the S group. Third generation MSCs with a concentration of 1×107/10 ml PBS were injected via the ear marginal vein immediately at injury into the M group. VEGF in peripheral blood and lung tissue were measured at 0 （baseline）, 2, 4 and 6 hours after injection respectively and analyzed. The right lungs of rabbits were taken to measure lung water mass fraction.RESULTS： In the lung tissue, VEGF decreased gradually in the S group （P〈0.05） and signi？ cantly decreased in the M group （P〈0.05）, but it increased more signi？ cantly than the values at the corresponding time points （P〈0.05）. In peripheral blood, VEGF increased gradually in the S group （P〈0.05） and markedly increased in the M group （P〈0.05）, but it decreased more signi？ cantly than the values at corresponding time points （P〈0.05）.CONCLUSION： MSCs engraftment to smoke inhalation injury could increase VEGF in lung tissue, decrease VEGF in plasma and reduce extravascular lung water, indicating its protective effect on smoke inhalation injury.

Effects of tetrandrine on the changes of free calcium level in neutrophils after smoke inhalation injury in the rabbit

The changes of the cytoplasmic free calcium level in the neutrophils after smoke in-halation injury were observed in rabbits and then the effects of tetrandrine,a calcium antago-nist,on the changes of free calcium level were studied.It was found that the number of neu-trophils increased significantly preceded by a transient decrease in the blood and also increasedin the bronehoalveolar lavage fluid after smoke inhalation.and the level of cytoplasmic free calci-um in the blood neutrophil increased likewise.Administration of tetrandrine resulted in a reduc-tion of the neutrophils number in the lungs and the free calcium level in the blood neutrophils toalleviate the pulmonary injury due to smoke inhalation.It is believed that there is a close rela-tionship between the activation of neutrophils and the pathophysiological changes of the lungs,and tetrandrine can exert its therapeutic effects on the injury by decreasing the free calcium levelin the neutrophils to modulate their functions.

The Effects of Ginsenosides on Smoke Inhalation Injury in Rats

A rat model was used to explore the therapeutic effects of ginsenosides (GS)on smoke inhalation long injury.It was found that GS could markedly alleviate the in-crease of pulmonary microvascular permeability (PMVP),reduction of protein and leu-cocyte content in the bronchoalveolar lavage fluid (BALF) of the smoke inhalation injur-ed rats.Histopathological studies of the lungs revealed that GS could distinctly reduceleucocyte accumulation in the vessels,interstitial infiltration of leucocytes,interstitial andintra-alveolar edema,hemorrhage and vascular congestion.Meanwhile,GS could inhibitthe elevation of malondialdehyde (MDA) in the lungs and serum and reverse the decrea-sed activity of superoxide dismutase (SOD) in the lungs after smoke inhalation.In addi-tion experiments in vitro also showed the inhibition of lipid peroxidation in lung homo-genate and elimination of superoxide anions hydroxyl radicals effectively by GS in properdoses.These results imply that there is close interrelationship between the therapeuticefficiency of GS on smoke inhalation lung injury and its capability of antioxidation.

The Protective Effects of Preventive Atomisation Inhalation of Edaravone on the Lung Tissues of Rats with Smoke Inhalation Injury

Objective: To investigate the protective effects of the atomisation inhalation of edaravone on the lung tissues of rats with smoke inhalation injury. Methods: Forty male Sprague-Dawley (SD) rats were randomly divided into four groups of ten rats each: normal control group (group A), normal saline atomisation group (group B), edaravone aerosol group (group C) and edaravone atomisation prevention group (group D). Barring group A, the groups were used to create a model of severe smoke inhalation injury. However, before developing the model, group D rats were made to inhale edaravone (3.6 mg/mL) for 10 min. Six hours following smoke inhalation injury, abdominal artery blood samples were centrifuged, the lung tissue homogenate was prepared and carotid artery blood samples were used for blood gas analysis and oxygenation index (PaO2/FiO2) calculation. The levels of tumour necrosis factor alpha (TNF-α), interleukin (IL) 6 and IL-10 in serum and the levels of cysteine protease 3 (caspase-3), malondialdehyde (MDA), myeloperoxidase (MPO) and superoxide dismutase (SOD) in lung tissues were examined. The wet-dry ratio (W/D) and water content of the lung tissue were calculated, and the TUNEL method was used to determine the rate of lung tissue apoptosis in each group. Tissue specimens were obtained from the partial lung for histopathological examination. Results: Compared with those in group A, the water content of the lung tissue, the rate of lung tissue apoptosis, W/D and the caspase-3, TNF-α, IL-6, IL-10, MDA and MPO levels were significantly greater in other groups (PP< 0.05). Compared with those in group B, the levels of W/D, the water content of the lung tissue, the rate of lung tissue apoptosis and the levels of caspase-3, TNF-α, IL-6, MDA and MPO were significantly low (P and the levels of IL-10, SOD and PaO2/FiO2 were significantly high in groups C and D (P The expression of the aforementioned factors was more evident in Group D (P < 0.05). Histopathological examination revealed that groups C and D had greater levels of inflammatory granulocytes than group B. This was more evident in group D. Conclusions: The inhalation of edaravone can reduce smoke inhalation-induced lung injury. This may be related to the inhibition of apoptosis, the reduction of peroxidation injury and the production/release of inflammatory mediators/free radicals. It exerts a remarkable preventive effect.

Pharmacological treatment of inhalation injury after nuclear or radiological incidents: The Chinese and German approach

Inhalation injury is often associated with burns and significantly increases morbidity and mortality. The main toxic components of fire smoke are carbon monoxide, hydrogen cyanide, and irritants. In the case of an incident at a nuclear power plant or recycling facility associated with fire, smoke may also contain radioactive material. Medical treatments may vary in different countries, and in this paper, we discuss the similarities and differences in the treatments between China and Germany. Carbon monoxide poisoning is treated by 100% oxygen administration and,if available, hyperbaric oxygenation in China as well as in Germany. In addition, antidotes binding the cyanide ions and relieving the respiratory chain are important. Methemoglobin-forming agents(e.g., nitrites, dimethylaminophenol)or hydroxocobalamin(Vitamin B12) are options. The metabolic elimination of cyanide may be enhanced by sodium thiosulfate. In China, sodium nitrite with sodium thiosulfate is the most common combination. The use of dimethylaminophenol instead of sodium nitrite is typical for Germany, and hydroxocobalamin is considered the antidote of choice if available in cases of cyanide intoxications by fire smoke inhalation as it does not further reduce oxygen transport capacity. Systematic prophylactic use of corticosteroids to prevent toxic pulmonary edema is not recommended in China or Germany. Stable iodine is indicated in the case of radioiodine exposure and must be administered within several hours to be effective. The decorporation of metal radionuclides is possible with Ca(DTPA)or Prussian blue that should be given as soon as possible. These medications are used in both countries, but it seems that Ca(DTPA) is administered at lower dosages in China. Although the details of the treatment of inhalation injury and radionuclide(s) decorporation may vary, the general therapeutic strategy is very similar in China and Germany.

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 PGI2 level was elevated and TXA2/PGI2 ratio decreased significantly.

Effects of Cigarette Smoke Extract on E-cadherin Expression in Cultured Airway Epithelial Cells

Summary: To investigate whether the change of E-cadherin (ECD) expression plays a role in the injury and repair of airway epithelial cells (AEC) caused by smoking, porcine AECs were cultured by using an enzyme-dispersed method. After exposure of the AECs to cigarette smoke extract (CSE), the ECD expression in the cells was detected by using immunocytochemistry and in situ hybridization. The results showed that ECD was distributed on the plasma membrane at the cell junctions of AECs. After exposure to 20 % CSE, the membranous ECD expression was decreased, the cytoplasmic ECD expression was increased (P<0.01) as the exposure time went on. But the content of ECD mRNA in the AECs did not chang. It suggests that the change of ECD ex- pression is regulated at the posttranslational level and plays a role in the injury and repair of AEC caused by smoking.

Dexamethasone up-regulates TNFAIP3 to attenuate inflammatory response with smoke inhalation-induced acute lung injury based on the GEO database

To explore the protective effect of dexamethasone(Dex)on early inflammation in mice with smoke inhalation-induced acute lung injury(SI-ALI),we screened and analyzed bioinformatics gene chip data,followed by laboratory verification.The GEO database was used to search the ALI gene datasets,which were processed by the GEO2R online tool.The differential genes of each dataset were analyzed by Venn diagram to select the differential genes.A protein-protein interaction network was built on the String platform,and key protein modules were screened with Cytoscape software.The online databases DAVID and KOBAS were used for GO and KEGG enrichment analyses.A total of 45 C57BL/6 mice were randomly divided into three groups as follows:control group,smoke inhalation group(smoke group),and smoke inhalation+Dex group(smoke+Dex group),with 15 in each group.Inhalation of smoke for 10 min caused SI-ALI in the smoke group and smoke+Dex group,and the air was given in the control group.Dex(0.4 mg/100 g)was injected in the smoke+Dex group.Animals were sacrificed 24 h later,the bronchoalveolar lavage fluid(BALF)of the left lung was collected,and the levels of IL-1βand IL-6 were detected by ELISA.The expressions of mitogen-activated protein kinase kinase kinase 8(MAP3K8)and tumor necrosis factor-alpha-induced protein 3(TNFAIP3)in the right middle lobe were measured by real-time fluorescent quantitative PCR.GSE1871,GSE2411,and GSE17355 gene datasets were included,and 60 differential genes were selected.The key modules mainly included IL-6,IL-1β,MAP3K8,and TNFAIP3.The biological process of GO was mainly concentrated in inflammation,immune response,and so on.Cell components were mainly concentrated in extracellular and molecular functions.KEGG was mainly concentrated in TNF,Toll-like receptors,and NOD-like receptor signaling pathways.Compared with the control group,the levels of IL-1βand IL-6 in BALF in the smoke group and smoke+Dex group were significantly increased(all P<0.05),and the levels of IL-1βand IL-6 in the smoke+Dex group were lower compared with the smoke group(all P<0.05).Compared with the control group,the expressions of TNFAIP3 and MAP3K8 in the smoke group and smoke+Dex group were increased significantly(all P<0.05),and the expression of TNFAIP3 in the smoke+Dex group was increased compared with the smoke group(t=5.701,P<0.01).Moreover,the expression of MAP3K8 was decreased(t=13.49,P<0.01).It could be concluded that inflammation signal pathways in lung tissues of SI-ALI mice were activated,the secretion of IL-1βand IL-6 was increased,and the expressions of MAP3K8 and TNFAIP3 were increased.Application of Dex could up-regulate TNFAIP3,down-regulate MAP3K8,and decrease the secretion of IL-1βand IL-6.Dex might inhibit MAP3K8 by up-regulating TNFAIP3,thereby negatively regulating the TNF/MAPK signaling pathway to reduce the inflammatory response of SI-ALI.

小胶质细胞铁死亡在烟雾吸入性脑损伤中的作用机制探讨

目的探究小胶质细胞铁死亡在烟雾吸入性脑损伤中的作用机制。方法将20只C57BL/6小鼠随机分为对照组(Control组)、烟雾吸入性损伤(SII)组、铁抑素治疗组(Fer-1组,2.5 mmol/kg Fer-1)、甲磺酸去铁胺治疗组(DFO组,200 mg/kg DFO),每组5只。Fer-1组和DFO组于造模后第1、3、5天分别腹腔注射Fer-1和DFO。第6天通过苏木素伊红(HE)染色、普鲁士蓝染色观察各组小鼠脑组织的病理变化。实时荧光定量逆转录PCR(RT-qPCR)检测脑损伤因子、炎性因子、铁死亡因子基因表达水平。双联吡啶比色法测定小鼠脑组织中铁含量。硫代巴比妥酸比色法测定小鼠脑组织脂质过氧化物(LPO)、丙二醛(MDA)含量。黄嘌呤氧化酶法测定小鼠脑组织超氧化物歧化酶(SOD)活性。二硫代二硝基苯甲酸(DTNB)直接法测定小鼠脑组织谷胱甘肽(GSH)含量。DMEM完全培养基培养BV2细胞,分为Control组、Erastin组(10μmol/L Erastin刺激)、Fer-1组(10μmol/L Erastin与5 mmol/L Fer-1同时刺激)、DFO组(10μmol/L Erastin与50 mmol/L DFO同时刺激)。24 h后,CCK-8法检测细胞活力变化,流式细胞术检测细胞凋亡情况,2,7-二氯荧光素二乙酸酯(DCFDA)检测细胞内活性氧(ROS)水平,线粒体红色荧光探针检测线粒体膜电位。结果与Control组相比,SII组小鼠脑组织出现明显铁沉积和炎症反应,脑组织脑损伤因子、炎性因子mRNA表达水平升高,乙酰辅酶A合成酶长链家族4(ACSL4)、核受体共激活因子4(NCOA4)mRNA表达水平升高,谷胱甘肽氧化酶4(GPX4)、溶质载体家族7成员11(SLC7A11)mRNA表达水平降低,小鼠脑组织GSH和SOD含量降低,LPO和MDA含量升高(P<0.05)。与SII组相比,Fer-1组和DFO组小鼠相应指标变化与上述相反(P<0.05),小鼠脑组织损伤减轻。BV2细胞实验结果显示,与Control组相比,Erastin组BV2细胞存活率下降、凋亡率升高(P<0.05),细胞内ROS水平升高,线粒体膜电位下降;与Erastin组相比,Fer-1组、DFO组细胞相应指标变化与上述相反(P<0.05),BV2细胞氧化损伤得到缓解。结论铁死亡抑制剂Fer-1和DFO能够抑制小胶质细胞铁死亡并缓解烟雾吸入性脑损伤。

吸入麻醉药的肺保护作用研究进展

急性肺损伤是外科手术后常见的并发症,其高发病率和死亡率促使人们不断探索预防和治疗措施。肺损伤是多种机制相互交叉、相互影响的结果,其中,最严重的肺损伤为急性呼吸窘迫综合征。近年来,吸入麻醉药的临床应用日益广泛,其在手术过程中不仅可以起到镇痛、镇静的作用,还可以对心、脑、肺、肾、肝等重要脏器起到一定的保护作用,为手术过程中的器官保护提供了新的思路和方法。目前,最常用的吸入麻醉药为七氟烷、异氟烷、地氟烷。深入探索吸入麻醉药的肺保护机制,将为临床实践和未来的研究提供理论依据。

微小RNA-195通过靶向抑制PH结构域富亮氨酸重复蛋白磷酸酶2表达参与香烟烟雾诱导急性肺损伤机制研究

目的:探究miR-195通过靶向抑制PH结构域富亮氨酸重复蛋白磷酸酶2(PHLPP2)表达参与香烟烟雾诱导急性肺损伤的机制。方法:选择90只健康小鼠,均分为A、B、C三组,使用香烟烟雾暴露建立小鼠急性肺损伤模型,A组为正常对照组,B组为低剂量干预组,C组为高剂量干预组,干预后检测三组小鼠肺泡灌洗液中肿瘤坏死因子(TNF-α)、白介素-8(IL-8)及基质金属蛋白酶9(MMP-9)水平,对比三组小鼠肺泡灌洗液中白细胞、中性粒细胞计数,对比三组小鼠肺组织中髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)及谷胱甘肽(GSH)水平,最后检测三组小鼠肺组织中miR-195及PHLPP2蛋白表达量。结果:①肺泡灌洗液中TNF-α、IL-8及MMP-9水平C组>B组>A组,组间对比差异具有统计学意义(均P<0.05);②肺泡灌洗液中白细胞、中性粒细胞计数C组>B组>A组,组间对比差异具有统计学意义(均P<0.05);③肺泡灌洗液中MPO、SOD、GSH水平C组>B组>A组,组间对比差异具有统计学意义(均P<0.05);④肺组织中miR-195表达C组>B组>A组,PHLPP2蛋白表达C组<B组<A组,组间对比差异具有统计学意义(均P<0.05)。结论:香烟烟雾能够诱导小鼠肺组织出现炎性改变,其机制可能与miR-195过表达并抑制PHLPP2蛋白表达有关。

全氟化碳雾化吸入对大鼠海水吸入性肺损伤治疗作用研究

背景海水吸入性肺损伤是呼吸系统危重症,致死率高,目前缺乏有效治疗方法。全氟化碳(perfluorocarbon,PFC)是一种无色无味呈惰性的有机化合物,在多种急性肺损伤动物模型中表现出抗炎、抗氧化、减轻肺损伤等作用,目前无PFC雾化吸入对海水淹溺导致的急性肺损伤干预作用的研究。目的本研究拟探讨PFC雾化吸入对海水吸入性肺损伤的治疗作用。方法32只雄性SD大鼠随机分为4组,分别为0.9%氯化钠注射液组(N组)、全氟化碳雾化吸入组(P组)、海水吸入+0.9%氯化钠注射液吸入组(SW组)、海水吸入+PFC雾化吸入组(SP组),每组8只。SW组和SP组在建立海水吸入性肺损伤模型后30 min,分别经气管给予0.9%氯化钠注射液(2 mL/kg)和PFC(2 mL/kg)雾化吸入。于建模后4 h取肺组织、外周血和肺泡灌洗液,检测组织病理学、炎症指标[肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、白细胞介素(interleukin,IL)-1β、IL-6]、氧化应激指标[髓过氧化物酶(myeloperoxidase,MPO)、丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)]、肺湿干比、肺泡灌洗液蛋白浓度,取右下肺做HE染色。另取16只雄性SD大鼠,分为4组,每组4只(各组处理方式同上),各组于处死前30 min经右侧股静脉注射2%伊文斯蓝染料(20 mg/kg),测定肺组织伊文斯蓝含量。结果与N组相比,SW组肺损伤较重,肺损伤病理评分较高(P<0.05),血清及肺泡灌洗液TNF-α、IL-1β、IL-6、MDA、MPO、肺组织湿干比、肺泡灌洗液蛋白含量及肺组织伊文斯蓝水平显著升高(P<0.05),SOD含量降低(P<0.05)。海水吸入后给予PFC雾化吸入,可显著降低肺损伤病理评分、血清及肺泡灌洗液TNF-α、IL-1β含量、肺泡灌洗液IL-6、血清MDA、蛋白含量、湿干比、肺组织伊文斯蓝含量(P<0.05),SOD含量显著升高(P<0.05),而血清IL-6、MPO在SW组与SP组间无统计学差异。结论全氟化碳雾化吸入可显著减轻大鼠海水吸入导致的肺损伤,其机制可能与改善肺内炎症反应、氧化应激和肺泡毛细血管通透性有关。

吸入骨髓间充质干细胞来源外泌体减轻慢性阻塞性肺疾病的炎性损伤

背景:研究表明骨髓间充质干细胞源外泌体在多种呼吸系统炎症及疾病损伤模型中表现出强大的修复和再生能力,但在慢性阻塞性肺疾病中的研究较少,且尚未有研究将外泌体雾化吸入应用于慢性阻塞性肺疾病的模型实验中。目的:探讨大鼠骨髓间充质干细胞源外泌体通过雾化吸入途径对慢性阻塞性肺疾病大鼠炎症和肺部损伤的治疗作用,并且明确最适治疗剂量。方法:体外分离培养大鼠骨髓间充质干细胞,并提取鉴定其外泌体。脂多糖联合烟熏28 d建立慢性阻塞性肺疾病大鼠模型,然后给予低剂量(0.5×10^(8)particles/kg)、中剂量(1.0×10^(8)particles/kg)、高剂量(1.5×10^(8)particles/kg)外泌体雾化吸入治疗以及外泌体(1.5×10^(8)particles/kg)尾静脉注射治疗,模型组雾化1 mL PBS,对照组不造模、雾化1 mL PBS。连续雾化或注射治疗5 d,最后一次雾化或注射治疗后的第2天开始检测,使用小动物肺功能仪测试各组肺功能指标,ELISA检测支气管肺泡灌洗液及血清中的白细胞介素1β和肿瘤坏死因子α水平,苏木精-伊红染色和Masson染色从组织学评估肺组织改变。结果与结论:①骨髓间充质干细胞来源外泌体在透射电镜下显示为椭圆形的双层膜囊泡结构,呈典型的杯口状,粒径分析提示外泌体的峰直径为91.7 nm,占比为97.3%,颗粒浓度为3.3×10^(9) L^(-1),并且外泌体表面蛋白CD9和CD63高表达;②与尾静脉注射外泌体相比,雾化吸入外泌体显著改善了慢性阻塞性肺疾病大鼠的肺功能、肺组织切片胶原沉积和肺组织病理变化,并且明显降低了支气管肺泡灌洗液和血清中白细胞介素1β和肿瘤坏死因子α水平,且低剂量外泌体治疗效果最为显著;③以上结果表明,雾化吸入骨髓间充质干细胞来源外泌体可以减轻慢性阻塞性肺疾病的炎性损伤,并且最适剂量可能为0.5×10^(8)particles/kg。

小鼠烟雾吸入性损伤模型的建立与评估

背景吸入性损伤最常见为高温、有毒烟雾导致的损伤,然而关于其致病机制的研究仍不明确。目的研发一种简便易得的新型小鼠烟雾吸入性损伤模型,观察小鼠生理状态、组织病理学变化以及炎性因子改变。方法160只C57BL/6小鼠随机选取20只作为对照组,其余140只小鼠随机分为4组。采用自制烟雾致伤装置,以胶合板和松木屑作为发烟材料,实验组分别进行10 min、15 min、20 min、25 min烟雾吸入致伤,对照组小鼠不经烟雾吸入。观察烟雾吸入性损伤后小鼠行为状态、生理表现以及72 h生存变化情况;各组小鼠处死后取肺组织,观察其病理改变、干湿重改变及检测组织细胞内蛋白和炎性因子含量。结果致伤10 min、15 min、20 min、25 min后72 h生存率分别为100%、83%、54%和0,其中25 min致伤组小鼠在伤后12 h内全部死亡。与对照组相比,各致伤组小鼠伤后出现呼吸急促、活动减少,随后部分自行恢复至正常状态,部分进食进水减少,状态萎靡;主要观察致伤20 min组小鼠肺部病理组织,可见炎性细胞浸润,肺泡结构破坏,肺泡隔增厚;干湿重显示有肺水肿出现,伤后12 h和24 h小鼠肺组织匀浆炎性因子检测白细胞介素(interleukin,IL)-1β、IL-6和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)与对照组相比显著上升,IL-10显著下降(P均<0.05)。结论吸入20 min由胶合板和松木混合燃烧产生的烟雾可以导致C57BL/6小鼠中重度吸入性损伤,伤后实验动物的生理表现和组织病理结果与临床病情相符。

术前雾化吸入盐酸戊乙奎醚对单肺通气时非通气侧肺损伤的影响及作用机制研究

目的探讨术前雾化吸入盐酸戊乙奎醚在减轻单肺通气(OLV)时非通气侧肺损伤的影响及作用机制。方法招募2021年3月至2022年5月于郑州大学附属洛阳中心医院择期行胸腔镜下肺癌根治术患者60例,采用随机数字表法将其分为观察组和对照组,每组30例。麻醉诱导后即刻,对照组予雾化吸入异丙托溴铵,观察组予雾化吸入盐酸戊乙奎醚。于全身麻醉诱导后即刻(T_(0)),以及OLV开始后0.5 h(T_(1))、1 h(T_(2))、2 h(T_(3))时检测血氧分压(PaO_(2))和二氧化碳分压(PaCO_(2))。术中切取肿瘤周边的正常肺组织标本进行病理学检查,计算肺损伤评分。采用TUNEL法计算细胞凋亡指数(AI)。采用Western blot法检测肺组织细胞凋亡和自噬标志性蛋白的表达水平。结果光镜下可见对照组肺组织形态、结构发生明显损伤,而观察组肺组织损伤显著减轻。在观察时间内,两组PaO_(2)均呈下降趋势,PaCO_(2)呈上升趋势,且观察组变化幅度较小(P<0.05),在T_(1)~T_(3)时间点与对照组比较差异有统计学意义(P<0.05)。与对照组比较,观察组肺损伤评分、AI、B淋巴细胞瘤-2相关X蛋白(Bax)、微管相关蛋白1轻链3(LC3)-Ⅱ、自噬标志性蛋白Beclin-1水平,以及LC3-Ⅱ/LC3-Ⅰ比值显著降低(P<0.05),而B淋巴细胞瘤-2(Bcl-2)、LC3-Ⅰ蛋白水平以及Bcl-2/Bax比值均显著升高(P<0.05)。结论术前雾化吸入盐酸戊乙奎醚可减轻OLV时的非通气侧肺损伤,而肺组织细胞凋亡及自噬的抑制在其中具有重要作用。

分级气道护理在成批烟雾吸入性损伤患者中的应用效果及对情绪、睡眠状态的影响

目的:探究分级气道护理在成批烟雾吸入性损伤患者中的应用效果及对情绪、睡眠状态的影响。方法:将2019年6月—2022年2月中国人民解放军联勤保障部队九一〇医院的80例成批烟雾吸入性损伤患者根据随机数字表法分为对照组和观察组,各40例。对照组进行常规护理,观察组则进行分级气道护理。比较两组的后遗症发生情况、干预前后的损伤情况[支气管镜简明损伤(AIS)评分]、情绪状态[焦虑自评量表(SAS)评分及抑郁自评量表(SDS)评分]及睡眠状态[匹兹堡睡眠质量指数(PSQI)]。结果:6个月后,观察组的后遗症发生率显著低于对照组,差异有统计学意义(P<0.05)。干预前两组的AIS评分、SAS评分、SDS评分及PSQI评分比较,差异均无统计学意义(P>0.05)。干预后1周及3周两组的AIS评分、SAS评分、SDS评分及PSQI评分均显著优于干预前,且观察组的上述评分均显著优于对照组,差异均有统计学意义(P<0.05)。结论:分级气道护理在成批烟雾吸入性损伤患者中的应用效果较好,且可显著改善患者的情绪及睡眠状态。

依达拉奉与地塞米松联用对烟雾吸入性肺损伤大鼠呼吸功能及肺组织形态的影响

目的探讨依达拉奉与地塞米松联用对烟雾吸入性肺损伤大鼠呼吸功能及肺组织形态的影响。方法将50只SD大鼠随机分为空白对照组(C组)、烟雾染毒对照组(M组)、依达拉奉组(E组)、地塞米松组(D组)、联合用药组(ED组),各10只。除C组外,其他组大鼠在产烟浓度为25mg/L的条件下连续染毒30min,1h后给予药物干预。E组大鼠腹腔注射依达拉奉5mg/kg,D组大鼠腹腔注射地塞米松5mg/kg,ED组大鼠同时给予相同剂量的依达拉奉和地塞米松。24h后检测所有大鼠呼吸功能并分析血气,取左肺组织HE染色后作病理学检查,取右肺下叶组织测肺组织湿干比(W/D)。结果染毒后,大鼠的呼吸频率(f)、潮气量(TV)、分钟通气量(MV)明显降低,吸气时间(Ti)和呼气时间(Te)明显增加。单用或联合给药后呼吸功能的异常改变均有不同程度的恢复,肺组织的W/D明显降低,血液pH、氧分压(PaO_(2))、氧饱和度(SO_(2))升高,二氧化碳分压(PaCO_(2))明显降低。联合用药组的肺组织病理损伤缓解最明显。结论依达拉奉与地塞米松单用或联用均可以改善烟雾吸入导致的大鼠呼吸功能损伤和肺组织形态改变,其中联合用药对于改善肺组织病理损伤效果最明显。

分级气道护理对成批烟雾吸入性损伤患者希望水平、效能感状态及生存质量的影响

目的:探究分级气道护理对成批烟雾吸入性损伤患者希望水平、效能感状态、生存质量的影响。方法:选择2020年3月—2022年3月中国联勤保障部队第九一〇医院收治的80例成批烟雾吸入性损伤患者为研究对象,根据随机数表法分为对照组和观察组,各40例。对照组进行常规吸入性损伤护理,观察组则进行分级气道护理干预。比较两组护理前后的希望水平(Herth希望量表)、效能感状态[一般自我效能感量表(GSES)]及生存质量[世界卫生组织生存质量量表(WHOQOL-100)]及患者对护理模式的总满意率。结果:护理前,两组Herth希望量表、GSES量表及WHOQOL-100量表评分比较,差异无统计学意义(P>0.05)。护理1周、2周、3周后,两组Herth希望量表、GSES量表及WHOQOL-100量表结果均优于护理前,且观察组的上述结果均显著优于对照组,差异有统计学意义(P<0.05)。观察组护理总满意率显著高于对照组,差异有统计学意义(P<0.05)。结论:分级气道护理可显著改善成批烟雾吸入性损伤患者的希望水平、效能感状态及生存质量,更受患者认可。

Influence of moxa smoke on mitochondrial transmembrane potential and Bax/Bcl-2 in alveolar type Ⅱ epithelial A549 cells

Objective： To investigate the influence of moxibustion products on mitochondrial transmembrane potential （MTP） and mRNA expression of Bax/Bcl-2 in alveolar type Ⅱ epithelial A549 cells, and to further explore influence of moxibustion products on the oxidative damage of A549 cells. Methods： Smoke and particles generated by moxibustion were collected using the filter box for gas sampling. The moxa smoke extract （MSE） was diluted sequentially to the final concentrations of 0.05 mg/mL, 0.2 mg/mL, 0.2 mg/mL, 0.3 mg/mL and 0.4 mg/mL using the cell culture medium, and A549 cells were then intervened by the above MSE solution. Cell MTP was detected by JC-1 staining. Fluorescence quantitative polymerase chain reaction （PCR） was used to detect Bax/Bcl-2 mRNA expression of A549 cells. Results： Compared with cells in the normal control group, MTP was significantly decreased in cells of 0.3 mg/mL and 0.4 mg/mL MSE intervention groups （P〈0.01）; while MTP showed no significant changes in cells of 0.05 mg/mL, 0.1 mg/mL and 0.2 mg/mL MSE intervention groups （P〉0.05）; compared with cells in 0.05 mg/mL MSE intervention group, MTP was decreased significantly in cells of 0.1 mg/mL, 0.2 mg/mL, 0.3 mg/mL and 0.4 mg/mL MSE intervention groups （P〈0.05）; compared with cells in 0.1 mg/mL MSE intervention group, MTP was decreased significantly in cells of 0.4 mg/mL MSE intervention group （P〈0.01）. Bax mRNA expression of cells in each concentration of MSE intervention group all showed no significant difference compared to that in the normal control group; Bcl-2 mRNA expression of cells was reduced with the increase of MSE intervention concentration. Wherein, Bcl-2 mRNA expressions of cells in 0.4 mg/mL and 0.3 mg/mL MSE intervention groups were significantly reduced compared with that of cells in the normal control group （P〈0.05）; Bcl-2 mRNA expression of cells in 0.4 mg/mL MSE intervention group was significantly reduced compared to that in 0.05 mg/mL MSE intervention group （P〈0.05）. Conclusion： Certain higher concentration of moxa smoke could reduce MTP and mRNA expression of the anti-apoptosis gene Bcl-2 in alveolar type Ⅱ epithelial A549 cells. Oxidative damage may be the important mechanism of apoptosis caused by the high concentration of moxa smoke solution, and further studies are necessary on the specific mechanisms.