高过载后不同时期恒河猴心脏损伤的病理形态学观察

载人飞船在上升和返回时，航天员会遇到较为强大的胸一背向超重（＋Gx）压力的作用。特别是飞船在主动段大气层外弹道式应急返回时，过载峰值可高达15G甚至20G以上。以往的研究表明，＋Gx作用对人体肺脏和呼吸功能的影响最为突出，除可引起呼吸困难、胸痛等症状外，还可导致咯血、气胸等病理性损伤，但有关＋Gx过载作用后胸腔脏器，特别是有关心脏所呈现的损伤性病理变化和机制目前未见报道。吴斌等研究了＋Gx作用对大鼠膈肌收缩性能的影响及其机理，从而揭示了＋Gx导致大鼠膈肌疲劳的原因可能与＋Gx作用下缺血缺氧引起的膈肌能量代谢和超微结构的改变有关。     

动物慢性肺泡气肿的病因与诊治

动物慢性肺泡气肿是因肺泡持续性扩张，导致肺泡壁弹性丧失，造成肺泡壁、肺间质及弹力纤维萎缩，甚至崩解的慢性肺脏疾病。在临床上，动物一般以高度呼吸困难，肺泡呼吸作用减弱及肺脏叩诊界后移为主要特征。本病常见于马、骡等马属动物，役用牛、猎犬也可能发生，但相对较为少见。     

昆明小鼠心源性肺水肿肺脏组织超微结构病理变化的研究

为了研究小鼠心源性肺水肿肺脏组织超微结构的病理变化,试验以昆明小鼠为模型动物,通过腹腔注射不同剂量的肾上腺素导致小鼠产生心脏和呼吸系统血液循环障碍,然后采用病理解剖学、病理组织学和超微病理学的检测方法对试验小鼠的肺脏组织结构进行观察,以确定心源性肺水肿肺脏组织结构的变化。结果表明:病理组织学检查可见,小鼠支气管管壁间隙增宽,血管扩张,红细胞积聚;肺泡管腔狭窄,炎性细胞浸润,肺泡扩张、气肿等缺氧变化。电镜观察可见,小鼠支气管上皮肿胀,气管内有红细胞和浆液产生;支气管黏膜肿胀增厚,气管黏膜表面纤毛断裂、脱落;病变肺泡中隔断裂,肺泡融合扩张,肺泡体积增大。说明将剂量为0.01~0.03 m L/g的肾上腺素注射到小鼠体内均可导致小鼠死亡。     

人工感染兔支气管败血波氏杆菌的病理形态学观察

为研究兔支气管败血波氏杆菌致病机理及病理特征,对3月龄的家兔以1.5×1012cfu剂量滴鼻感染,观察家兔发病临床表现及死亡后病理变化。剖检并采集感染死亡后家兔各器官观察制作切片及组织学染色。结果显示家兔临床表现咳嗽、呼吸困难,窒息而死;死亡家兔剖检表现呼吸系统病变严重,主要为小叶性肺炎,气管黏膜充血和少量出血点;病理组织学表现为局部肺脏组织充出血及水肿,肺泡巨噬细胞显著增生,肺泡腔内充满浆液纤维素性渗出物和大量的嗜中性粒细胞,细支气管黏膜上皮脱落,周围可见淋巴细胞浸润。通过验证表明,败血波士杆菌主要引起肺脏病变,最终导致窒息死亡。     

人工感染兔支气管败血波氏杆菌的病理形态学观察

为研究兔支气管败血波氏杆菌致病机理及病理特征,对3月龄的家兔以1.5×1012cfu剂量滴鼻感染,观察家兔发病临床表现及死亡后病理变化。剖检并采集感染死亡后家兔各器官观察制作切片及组织学染色。结果显示家兔临床表现咳嗽、呼吸困难,窒息而死;死亡家兔剖检表现呼吸系统病变严重,主要为小叶性肺炎,气管黏膜充血和少量出血点;病理组织学表现为局部肺脏组织充出血及水肿,肺泡巨噬细胞显著增生,肺泡腔内充满浆液纤维素性渗出物和大量的嗜中性粒细胞,细支气管黏膜上皮脱落,周围可见淋巴细胞浸润。通过验证表明,败血波士杆菌主要引起肺脏病变,最终导致窒息死亡。     

槐山羊链球菌与巴氏杆菌混合感染的诊疗

今年夏初，我县新安集镇李某购进槐山羊１０只，未经任何检疫。不久，该批羊突然发病，发病５日后出现死亡，至第７日死亡４只。综合临床症状、病理剖检变化和细菌学分离鉴定，确诊为羊链球菌巴氏杆菌混合感染，通过紧急救治使疫情得到了及时控制。１ 临床症状 主要表现为精神沉郁，体温４１℃以上；眼结膜初期潮红有出血点，后期则极度苍白；鼻有出血和浆液性鼻漏，呼吸困难，伴有呻吟；颌下淋巴结肿大，部分羊出现头肿，并伴有抽搐、磨牙等神经症状；粪便初期稀薄，后期干燥并带有暗红色粘液；四肢内侧、腹部及尾下皮肤有出血点、斑，孕羊…     

犬瘟热鉴别诊治(三)

2．2 组织学检查 患犬肺脏广泛瘀血、水肿，肺泡壁增厚、细胞增多。部分肺泡腔中充满浆液、嗜中性粒细胞、巨噬细胞和脱落的肺泡上皮细胞，有些部位的肺泡壁坏死、溶解。患犬支气管和细支气管上皮细胞坏死、脱落．固有膜内有嗜中性粒细胞浸润，管腔中充积多量化脓性渗出物。少数病犬支气管和细支气管上皮细胞浆中可见嗜酸性病毒包涵体。     

运输应激对小鼠肺脏显微和超微结构及热休克蛋白表达的影响

为阐明运输应激对小鼠肺脏的病理损伤及热休克蛋白表达的影响,本实验运用HE染色、醋酸铀-枸橼酸铅染色、免疫组织化学染色和图像分析等方法,分析运输应激小鼠显微结构、超微结构以及HSP27、HSP70和HSP90表达的变化情况。结果表明:运输应激小鼠肺泡腔塌陷或发生融合,肺泡腔中可见脱落的细胞及胞质内容物,肺泡隔增厚,毛细血管明显扩张,炎性细胞浸润,肺泡Ⅰ型和Ⅱ型上皮细胞均发生明显的超微病理损伤,部分细支气管上皮脱落;与对照组相比,运输应激小鼠肺脏HSP27蛋白表达未见明显变化,HSP70蛋白表达量是对照组的10倍(P0.01),HSP90蛋白表达量下降。综上可知,运输应激对小鼠肺脏组织结构造成较大损伤,细胞病变较明显,HSP70和HSP90蛋白与肺脏应激损伤的发生发展存在一定的关联。     

猪繁殖与呼吸综合征病毒SJ株(天津分离株)感染仔猪的病理学

选用10～15日龄健康仔猪20头，随机分为攻毒组（15头）与对照组（5头），攻毒组滴鼻接种猪繁殖与呼吸综合征病毒（PRRSV）SJ株，3mL／头；对照组滴鼻接种无PRRSV的细胞培养物，3mL／头。攻毒组的主要临床表现为眼睑水肿、打喷嚏、呼吸急促、嗜睡、体温略升高。攻毒组与对照组在试验开始后24h、7d、14d、21d、28d分别剖杀3头和1头仔猪，采集肺、脾、肾、扁桃体及各部位淋巴结作免疫组化及病理组织学观察；迅速采集肺组织，制作超薄切片，透射电镜观察。试验结果表明，PRRSV SJ株主要感染仔猪的肺脏与脾脏。免疫组化观察，攻毒后24h～7d，肺门淋巴结和扁桃体PRRSV抗原阳性反应最强；攻毒后14～28d，牌睦PRRSV抗原阳性反应最强。攻毒后14～28d，显微病变可见肺组织发生弥漫性、局灶性或间质性肺炎，肺泡隔因巨噬细胞、淋巴细胞及Ⅱ型上皮细胞增生而明显增厚。超微病变主要表现为，肺泡间隔中单核细胞增生，核孔消失，核内有异染色质聚集，Ⅱ型肺泡细胞高度变性等。     

喜鹊新城疫的诊治

1 剖检病变 死亡喜鹊肛门周围粘粪，死前有腹泻。拔去死喜鹊羽毛后见其肌肉呈暗红色，全身黏膜多有出血点，尤其是喉头黏膜及会厌软骨黏膜出血点明显。嗉囊内充满酸臭味，腺胃和肌胃空虚，腺胃黏膜有白色脓样黏液，刮去黏液后可清楚地看见腺胃乳头上有鲜红色的出血点和溃疡，特别是腺胃和肌胃交界处有大量的出血点，肌胃角质层下也有少量的出血点。十二指肠、空肠、回肠及直肠呈暗红色，剖开后可见大小不等的出血点，肠黏膜有纤维性坏死性病变，盲肠扁桃体肿大，有出血点。气管出血，肺水肿、呈粉红色。心冠脂肪有针尖大小的出血点，脾呈圆…     

栀子四黄散抗猪繁殖与呼吸综合征的研究

为探索栀子四黄散对猪繁殖与呼吸综合征（porcine reproductive and respiratory syndrome,PRRS）的治疗效果,本研究将45头组随机分为对照组、病毒组及中药高、中、低剂量组5组,每味中药400目超微粉碎后分别添加饲喂接种猪繁殖与呼吸综合征病毒（porcine reproductive and respiratory syndrome virus,PRRSV）的试验猪,连续饲喂14 d,每日观察临床症状,7、14和21 d时随机采集5组血清样品进行细胞因子检测,并进行病理剖检和采集肺脏样品进行病理组织切片观察。结果显示,添加中药7 d后临床症状均减轻,中剂量和高剂量组第14天时体温恢复正常,呼吸困难症状消失,食欲恢复,中药治疗组肺脏未见肉样变,肺脏表面有出血点或出血斑。中剂量组肺泡间隔增厚,轻度淤血,肺实质轻度炎性细胞浸润。病毒组猪血清中IgG和γ-干扰素（IFN-γ）含量逐渐降低,白介素-10（IL-10）含量逐渐上升。添加中药的3组血清中IgG含量均高于病毒组,并且IgG含量均随时间延长逐渐上升,中剂量组血清中IgG含量均极显著高于对照组和病毒组（P<0.01）;添加中药的3组IFN-γ含量逐渐上升,14和21 d时中剂量组血清中IFN-γ含量均极显著高于对照组和病毒组（P<0.01）;中剂量组血清中IL-10含量逐渐降低,14和21 d时与病毒组差异极显著（P<0.01）,与对照组差异不显著（P>0.05）。综上,栀子四黄散可有效改善试验猪临床症状、病理变化和细胞因子的分泌,中剂量组效果最好。本研究为中药防治PRRS提供了试验依据。     

二甲苯对小鼠肺组织损伤的初步研究

为了研究二甲苯对小鼠肺组织的损伤情况,以健康成年小鼠作为试验动物,分3个试验组(低、中、高剂量组)1个对照组,给试验组腹腔注射不同剂量二甲苯(0.125、0.25、0.5 mL/kg),给对照组腹腔注射生理盐水.15 d后剖检取材,采用石蜡切片和HE染色技术研究二甲苯染毒后小鼠肺组织结构的变化特点;采用分光光度法测定小...     

大剂量维生素A、K对仔猪肝肾功能影响的研究

120头30日龄仔猪饲喂基础日粮1周后,将其随机分为正常对照组,添加VitA组、VitK组、VitA VitK组,共4组;其日粮组成分别为基础日粮、1kg基础日粮 5000IU VitA、1kg基础日粮 5mg Vitk、1kg基础日粮 5000IUVitA 5mg VitK.在4周龄和8周龄末,每组心脏采血10头,检测添加VitA、VitK对肝、肾功能的影响.     

Pulmonary atherosclerosis and pulmonary arterial pressure in cholesterol-fed New Zealand white rabbits.

The lung produces many vasoactive substances originating from its vascular endothelium and plays an important part in various pathose. The present study was carried out to clarify pulmonary atherosclerosis and pulmonary arterial pressure, and to elucidate a part of the pulmonary pathosis in cholesterol-fed rabbits. Atherosclerosis was induced by feeding the animals a cholesterol-rich diet. When the rabbits were fed the cholesterol-enriched diets for 15 weeks, the grade of the atherosclerosis was severer than in 8W-feeding rabbits. The lesions of 8W-feeding rabbits were mainly composed of foam cells and fibrous components, whereas in 15W-feeding rabbits, the aggregation of foam cells beneath the endothelium of the vessel was infiltrating the media and severe stenose of the lumen was observed. In the entire pulmonary arterial system, the severe obstructive vascular lesions were localized and not diffused. The pulmonary arterial pressures of the rabbits increased slightly with time and the mean pressures were 11.3+/-0.9 (control group), 11.8+/-1.0 (8W group) and 13.7+/-1.5 mmHg (15W group) respectively. A significant difference existed in the mean pressure between the control group and 15W-feeding group, but there were no significant differences in the systolic and diastolic pressures among the three groups. In conclusion, we could induce pulmonary atherosclerosis in rabbits by feeding them a hyper-cholesterol diet but not overt pulmonary hypertension.     

气管给药法检测甲醛对小鼠肺组织氧化损伤的研究

为观察由甲醛引起的小鼠肺组织氧化损伤，采用气管给药法将不同剂量的液态甲醛通过气管直接给药，连续染毒处死后，摘取小鼠肺组织，测定肺表面活性物质相关蛋白A（SP-A）含量、肺组织SOD活力以及MDA含量；制作肺组织HE染色切片，观察小鼠肺组织病理变化。结果表明，高、低剂量组的SP-A含量及肺组织SOD活力均显著低于生理盐水对照组（P〈0.05），高、低剂量组的肺组织MDA含量均显著高于生理盐水对照组（P〈0.05）；光镜下观察可见高、低剂量组的肺泡间质细胞增多，且炎症细胞增多，发生炎性浸润。综上提示，甲醛可引起小鼠肺组织氧化损伤。     

高钠所致肺动脉高压肉鸡肺细小动脉病理改变的图象分析

240羽健康AA肉鸡随机均分为试验1组，试验2组和对照组，从8日龄起分别饮用含Na^ 为0.06%、0.12%和0.0%的饮水，其它饲养管理条件相同，分别于12、19、30、34、39日龄抽取各组参试鸡，以右心室（Right ventricle,RV)与全心室（Total ventrcle,TV)的重量比（RV／TV）作为判定肺动脉高压的依据，用图象分析仪对肺细小动脉病理变化作定量检测。结果表明：34、39日龄时，试验1组和试验2组管壁面积／管总面积和中膜厚度占外径百分值明显大于对照组，肺小动脉密度明显低，其RV／TV值均大于0.25，表明试验组肉鸡发生了肺动脉高压。由此可见，由高钠引起肉鸡肺细小动脉血管重构的病变可能参与了肺动脉高压的形成过程。     

Study on the Regulation of microRNA-124-3p on Lung Injury in Mice Infected with H1N1 Subtype Swine Influenza Virus

In order to study the regulatory effect of microRNA-124-3p(miR-124-3p) on lung injury caused by H1N1 subtype swine influenza virus (SIV) in mice,the expression vector of miR-124-3p adenovirus was constructed,and the miR-124-3p differentially expressed mouse models were induced by intravenous injection in the tail of mice which were divided it into three groups (overexpression,inhibition and control groups).48 h later,mice in each group were inoculated with H1N1 subtype SIV in the nasal cavity,with 10⁵ EID₅₀ (50 μL) per mouse.The average body weight change rate,pathological section observation and relative mRNA expression level of related inflammatory factors IL-1β,TNF-α and IL-6 in mice were observed for 14 consecutive days.The results showed that the pre-miR sequence and its sponge sequence had been successfully inserted into the shuttle plasmid of adenovirus,and co-transfected into 293A cells.Real-time PCR detection confirmed that compared with control group,the expression level of miR-124-3p in overexpression and inhibition groups were extremely significantly increased (P<0.01) and significantly decreased (P<0.05),respectively,indicating that the adenovirus expression vectors were successfully constructed.The rates of weight change of overexpression,inhibition and control groups were －5.5%,－12.4% and －8.6%,respectively.The alveolar wall of inhibition and control groups were thickened,in which there were a lot of lymphocyte infiltration,some of the alveoli showed fibrin exudation,and the pathological changes were more serious in the inhibition group,there were a lot of RBC infiltration in alveoli.There were only a little lymphocyte infiltration in overexpression group,and the lung tissue was normal.Compared with control group,the mRNA expression levels of IL-1β,TNF-α and IL-6 in overexpression group were significantly decreased (P<0.05);The mRNA expression levels of inflammatory factors in inhibition group were significantly increased (P<0.05).The results showed that miR-124-3p inhibited the expression of pulmonary inflammatory factors induced by H1N1 subtype SIV in mice,and also alleviated pathological injury of lung.     

microRNA-124-3p调控H1N1亚型猪流感病毒致小鼠肺损伤的研究

为研究microRNA-124-3p（miR-124-3p）对H1N1亚型猪流感病毒（swine influenza virus，SIV）感染小鼠所致肺损伤的调控作用，本试验构建miR-124-3p腺病毒表达载体，通过小鼠尾部静脉注射法构建miR-124-3p差异表达小鼠模型，试验分3组：过表达组、抑制组和对照组。48 h后，各组小鼠鼻腔接种H1N1亚型SIV，每只10⁵ EID₅₀（50 μL）。连续观察14 d，计算小鼠平均体重变化率、观察病理切片并测定相关炎症因子IL-1β、TNF-α和IL-6 mRNA相对表达量。结果显示，已成功将pre-miR序列及其sponge序列插入腺病毒的穿梭质粒，并将其共转染293A细胞。实时荧光定量PCR检测证实，与对照组相比，过表达组和抑制组小鼠黑色素瘤细胞miR-124-3p表达水平分别极显著升高（P<0.01）和显著降低（P<0.05），表明成功构建腺病毒表达载体。过表达组、抑制组和对照组小鼠体重变化率分别为－5.5%、－12.4%和－8.6%。抑制组和对照组均可见肺泡壁增厚，其间有多量淋巴细胞浸润，部分肺泡内出现纤维蛋白渗出，且抑制组病理变化更为严重，肺泡中还有大量的红细胞浸润；而过表达组仅有少量的淋巴细胞浸润，肺脏组织较正常。与对照组相比，过表达组检测的炎症因子IL-1β、TNF-α和IL-6 mRNA表达水平均显著降低（P<0.05）；抑制组炎症相关炎症因子mRNA表达水平均显著升高（P<0.05）。本试验结果表明，miR-124-3p对H1N1亚型SIV感染小鼠所致的肺脏炎症因子的表达具有抑制作用，同时能减轻肺脏病理损伤。     

Effects of furosemide on the racing times of horses with exercise-induced pulmonary hemorrhage

In 3 groups of horses with exercise-induced pulmonary hemorrhage (EIPH), comparisons of racing times and finishing positions were made between the 5 races before the horses were given furosemide and 5 races after furosemide administration. The horses were grouped according to 3 methods used to diagnose EIPH: group 1, observation of hemorrhage at the nostrils within 1 hour after a workout or race; group 2, observation of pulmonary hemorrhage only by endoscopic examination after a race or workout; and group 3, observation of hemorrhage at the nostrils during a race or immediately after a race. Group 4 horses were randomly selected horses running during the study period and were not given furosemide. The statistical method was analysis of covariance and the dependent variable was horses' time per distance. The study compared the 4 groups of horses, using the estimated value of the horses (less than or equal to +10,000 or greater than +10,000), and the horses' interaction in races 1 through 5 before and races 6 through 10 after furosemide treatment. The horses' times were adjusted by the relevant covariates, distance, track variant, and winning time per distance. Significant changes in horses' time per distance were not noticed when comparing values from races 1 through 5 with those in races 6 through 10 in group 1 horses.(ABSTRACT TRUNCATED AT 250 WORDS)