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采用醋酸铅灌胃于成年昆明小鼠,观察铅致小鼠肾脏的病理形态变化。取小鼠分为4组,分别为醋酸铅高、中、低剂量组(40、20、10mg/kg)、生理盐水阴性对照组,经口灌胃每天定时定量连续给药40d。取小鼠肾脏经甲醛固定,常规石蜡包埋切片,HE染色,显微镜下观察小鼠肾脏的组织形态。结果表明,各试验组肾皮质部小管上皮细胞肿胀,胞质疏松,染色浅,空泡变性,发生广泛性颗粒变性,部分肾小管上皮细胞嗜酸性坏死;高剂量组肾皮质部肾小管周围大量淋巴细胞浸润,肾小管上皮细胞表现明显的颗粒变性和嗜酸性坏死,肾小球体积萎缩,结构破坏,出现局灶性硬化;部分肾小管管腔内可见嗜酸性凝固物,肾小球毛细血管扩张充血;中剂量组病变相对较轻;而低剂量组无明显形态学异常。结果提示铅对小鼠肾脏有毒性作用,且随剂量增加损伤加重。 相似文献
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剑尾鱼硫酸铜急性中毒的病理学研究 总被引：5，自引：1，他引：4
通过对实验动物化的剑尾鱼进行急性硫酸铜中毒实验,在观察症状和剖检变化以后,对实验96h期间死亡鱼与96h后仍存活的鱼进行石蜡切片,HE染色,光学显微镜观察。主要眼观病变为肝脏水肿和白色坏死点;鳃丝肿胀,黏液分泌增多;肾脏肿胀,充血。显微病变为肝细胞水泡变性,严重坏死;鳃小片上皮细胞肿胀,脱落严重;有的鳃小片发生融合,整个鳃丝呈棒状化;肾小管上皮细胞空泡变性,间质有充血或网织细胞增多,细胞间噬铁血红素细胞增多;肝胰腺的胰腺细胞的酶原颗粒减少。 相似文献
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剖开福寿螺,在体视显微镜下取出其肾脏;常规法制作石蜡切片,HE染色后,观察福寿螺肾脏的组织结构,结果是:肾脏由肾小管和集合管组成;肾小管为单层立方细胞;肾小管上皮细胞内有浅棕色的折光小体。 相似文献
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《中国奶牛》2015,(6)
为观察维生素A缺乏对肉犊牛的组织病理学影响,应用常规石蜡切片技术,H.E染色,镜检观察肉犊牛的肝脏、肾脏、瘤胃、皱胃、十二指肠、空肠及结肠7个内脏器官的组织病理学变化。结果显示:肝脏的正常结构没有变化,主要病理变化是充血、淤血;肾脏肾小管上皮细胞呈现水样变性;瘤胃上皮细胞无明显变化;皱胃底腺细胞明显复层化;十二指肠绒毛上皮细胞细胞核裂解明显,空肠的肠绒毛上皮严重脱落,结肠绒毛脱落伴有静脉淤血。结果表明,维生素A缺乏对肉犊牛的上述器官的组织结构有不同程度的影响。本文旨在通过观察维生素A缺乏对肉犊牛部分组织器官的损伤变化,探索其病理特征,从而为及时对发病动物进行确诊、治疗提供形态学上的依据。 相似文献
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《动物医学进展》2021,42(9)
为了解感染猪繁殖与呼吸综合征病毒(PRRSV)仔猪肾脏组织的主要病变和病毒主要分布的细胞类型,试验取人工感染PRRSV JXA1株的仔猪肾脏组织制作石蜡切片,采用HE染色法观察其病理变化,采用免疫组织化学方法检测病毒GP5蛋白和N蛋白在肾脏组织内的分布。结果表明,感染仔猪的肾脏组织呈现广泛性充血和出血,大量的炎症细胞浸润;感染仔猪肾脏组织的免疫组织化学染色,PRRSV GP5蛋白和N蛋白呈广泛性阳性着色,阳性细胞包括肾小球毛细血管内皮细胞、肾小管周围毛细血管内皮细胞、肾小管上皮细胞和肾间质等。说明PRRSV感染仔猪病毒粒子能够侵入肾脏组织,感染肾血管内皮细胞和肾小管上皮细胞等。 相似文献
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利用组织病理学、免疫组织化学等方法,探讨大肠杆菌感染对实验兔肾脏的组织病理学损伤及诱导型一氧化氮合酶(iNOS)在肾脏组织内的分布。结果显示,与对照组相比,大肠杆菌感染组的肾脏出现明显的病理损伤:皮质区肾小球萎缩,肾小球周围的肾间质有大量的淋巴细胞浸润,肾小管上皮细胞变性坏死,偶尔可见肾小管管腔内出现蓝染的细菌团块;髓质区有局灶性坏死,肾小管上皮细胞脱离基底膜,间质增生纤维化、充血。免疫组织化学结果显示,感染组兔肾脏组织中的iNOS的表达极显著高于对照组(P<0.01),结果表明,大肠杆菌感染可引起兔肾脏组织结构明显的病理损伤,iNOS表达量上调说明一氧化氮(NO)在一定程度上参与了大肠杆菌引起的兔肾脏损伤过程。 相似文献
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Histological and ultrastructural studies of renal lesions in Babesia canis infected dogs treated with imidocarb 总被引：1，自引：0，他引：1
Histological and electron microscopic examinations of the kidneys of 8 dogs suffering from fatal, naturally acquired Babesia canis infection and nephropathy are presented. Seven animals were treated with imidocarb dipropionate on average 4.5 days prior to death. Severe anaemia was present only in 2 cases. Degenerative histological changes observed mostly in the proximal convoluted tubules included vacuolar-hydropic degeneration, necrosis and detachment of renal tubular epithelial (RTE) cells from the basement membrane. Necrotic debris occasionally formed acidophilic casts within the tubules. In some cases, necrosis of the whole tubule was observed. Haemoglobin casts in the tubules and haemoglobin droplets in RTE cells seldom appeared. No significant histological changes were seen in the glomeruli. Ultrastructural lesions in RTE cells included nuclear membrane hyperchromatosis, karyopyknosis, karyolysis, swelling or collapse of mitochondria with fragmentation of cristae and vacuolar-hydropic degeneration in the endoplasmic reticulum and microvilli. Nuclear oedema was also observed. Many RTE cells exhibiting necrosis collapsed. Vacuolar-hydropic degeneration and necrosis were also observed in the glomerular and interstitial capillary endothelium. The severe acute tubular necrosis described in this study is probably the result of hypoxic renal injury. Systemic hypotension leading to vasoconstriction in the kidneys might be the most important cause of renal hypoxia in B. canis infections, but anaemia may also contribute to inadequate oxygenation. Imidocarb should be applied with caution in patients with possible renal involvement until further data become available on its potential nephrotoxicity in dogs. 相似文献
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K Kobayashi C Itakura J Arikawa N Hashimoto 《Zentralblatt für Veterin?rmedizin. Reihe B. Journal of veterinary medicine. Series B》1991,38(9):657-664
Hemorrhagic fever with renal syndrome (HFRS) virus, strain SR-11 (SR) was inoculated intraperitoneally into specific-pathogen-free (SPF) newborn rats, from which the kidney lesions were examined pathologically. The infected rats revealed proteinuria on and after 16 days postinoculation (PI). Histologically, the epithelial cells of the renal tubules showed mild vacuolar and granular degeneration with cytoplasmic inclusion bodies (CIB) on and after 16 days PI. Ultrastructurally, a decrease in number of mitochondria and endocytic vesicles was recognized in the epithelial cells of the proximal renal tubules. Occasionally, both the proximal and distal renal tubular cells had CIB near well-developed Golgi apparatus on and after 13 days PI. Immunohistochemically, CIB were positive for anti-SR nucleocapsid antibody, but negative for anti-SR envelope protein antibody. From the results obtained here, it was concluded that the proteinuria in rats infected with HFRS virus resulted from an insufficiency of reabsorption in the proximal renal tubules, and that CIB consisted of the viral nucleocapsid protein. 相似文献
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猪繁殖与呼吸综合征病毒（PRRSV）是能引起仔猪高死亡率的疾病,给养猪业带来极大的经济损失。本研究对PRRSV感染仔猪肾组织的病毒定位及产生的超微病理变化进行观察,以期了解PRRSV对肾组织细胞以及血液循环的影响。主要采用透射电镜技术结合血清生化检测、免疫组织化学染色（IHC）,对仔猪感染PRRSV后肾组织进行超微病理学观察及分析。结果发现,PRRSV感染后引起肾组织损伤,病毒主要分布于肾小球、坏死的肾小管上皮细胞胞质及巨噬细胞胞质内;肾小球内足细胞足突广泛融合或微绒毛化,内皮细胞肿胀;肾小管上皮细胞线粒体肿胀、嵴断裂、溶解;间质炎性细胞浸润。PRRSV通过巨噬细胞内复制随血液扩散至肾组织,引起损伤;根据透射电镜观察结果,足细胞足突融合,肾小球血管内皮细胞损伤引起微血栓形成,说明PRRSV感染仔猪后影响了肾小球滤过率,同时,对肾血液微循环系统造成损伤。本研究为阐明PRRSV的感染致病机制提供理论基础。 相似文献
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Du Plessis EC Prozesky L Botha CJ 《Journal of the South African Veterinary Association》2011,82(3):144-149
Toxicity in cattle by the shrub Nolletia gariepina was induced experimentally by intraruminal administration of 3 g/kg dried, milled plant material as a single dose. The animals had to be starved for 24 hours before dosing, as dosing on a full rumen did not induce any signs of toxicity during 5 days of observation and clinical pathology monitoring. Clinical signs were not specific and varied according to the duration (acute versus subacute) of the toxicological process. Clinical pathological parameters indicated renal and to a lesser extent hepatic damage, with raised serum concentrations of urea, creatinine, aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT). Increased urinary sodium and potassium concentration and GGT activity, as well as proteinuria, were evident. Histological and electron microscopic examinations revealed acute renal tubular epithelial cell degeneration and necrosis, especially of the proximal convoluted tubules. Mild hepatocellular degeneration was also noticeable. 相似文献
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Pigs fed a ration, 25% of which was rice culture, of Aspergillus ochraceus lost weight or failed to gain and became depressed. Some pigs died and most developed subcutaneous edema, hydrothorax, hydroperitoneum, pulmonary atelectasis, edema of the mesentery and perirenal edema. Microscopic lesions in addition to edema were primarily renal and consisted of tubular degeneration and necrosis, hyaline tubular casts, interstitial fibrosis and tubular cell regeneration. The first change found after 3 days was cytoplasmic vacuolation of the convoluted and straight segments of the proximal tubules. Necrotic proximal tubules were found after 4 days and after 9 days degeneration and necrosis involved predominantly proximal tubular segments. Pigs fed a ration, 12.5% of which was rice culture, for 8 weeks did not develop perirenal edema but had firm kidneys. Extensive interstitial fibrosis of the cortical labyrinth was the principal change. Within the fibrous connective tissue, some tubules were necrotic and others were atrophied. 相似文献
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Morphological changes in response to 2-chloro-4-acetotoluidine (CAT) toxicity in the quail appeared in the form of progressive necrosis of the kidney, particularly the proximal tubular epithelial cells. Changes at 32 hr after the CAT administration included vacuolar degeneration, dilatation of distal tubules containing hyaline and granular casts, overt necrosis, and deposition of urate casts in collecting tubules. There were no striking histopathological changes in the liver at 24 hr. However, small focal necrotic lesions were seen 32 hr after the CAT administration. A 40% protection against the toxicity of CAT at the lower dose was seen in quail pretreated with phenobarbital. The protection offered by phenobarbital pretreatment was attributed to a quantitative shunting of CAT and/or its reactive metabolite along the microsomal-mediated metabolic pathway of the kidney responsible for their inactivation. Administration of reduced glutathione (GSH) to quail treated with CAT offered little protection against the toxicity. The quail treated with a toxic dose of CAT had an increased level of thiobarbituric acid (TBA) reacting products in the liver, with a concomitant decrease in GSH content. This suggests that lipid peroxidation may be involved in CAT-induced hepatic damage of quail. It was hypothesized that the depletion of protective GSH stores coincident with gradual shutdown of the protective peroxidase system of the kidney may occur in a more advanced stage of CAT toxicity in quail. This would then result in a severe disturbance in renal excretion of uric acid and in frank necrosis of renal tubules. 相似文献
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以SD大鼠为研究对象,采用一次性灌胃给药法进行米尔贝肟的急性毒性试验,研究了试验大鼠对米尔贝肟的毒性反应和病理变化.结果显示,米尔贝肟对SD大鼠具有雄雌差异性,半数致死量(LD50)分别为2002、1131 mg/kg·BW.大鼠急性中毒4h后,出现明显的临床症状,主要表现为共济失调、立毛、精神委靡、呼吸困难、食欲减退,且呈明显的量效关系.组织病理学变化主要为肝脏中央静脉淤血,肝索排列紊乱,肝细胞颗粒变性;肺淤血;肾小管上皮细胞和消化道黏膜上皮颗粒变性、坏死;脾脏淤血;大脑皮层血管炎症细胞浸润,边缘空泡化.根据WHO外源性急性毒性分级标准,米尔贝肟属低毒化学物.米尔贝肟急性中毒后会广泛损害大鼠肝、肺、肾和肠等多种组织器官,甚至引起这些组织器官的变性坏死,并可对神经组织造成一定的损伤. 相似文献
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Ochratoxin A and citrinin induced nephrosis in Beagle dogs. III. Terminal renal ultrastructural alterations 总被引：1，自引：0，他引：1
The extent and type of renal ultrastructural changes in Beagle dogs varied with the administration of ochratoxin A and citrinin alone and in the two dosage combinations. The three predominant changes were cytoplasmic vacuolation, myelin figure formation and lesions designated as cytoplasmic disarray. These changes were mainly of the endomembane system of the tubular epithelial cells. Cytoplasmic vacuoles were within proximal and distal tubules and collecting ducts and were most numerous in dogs given 10 mg/kg critrinin. Vacuolation of similar distribution, but less severe, was seen in renal tubular cells of dogs given the higher dose of the combined mycotoxins (0.2 mg/kg ochratoxin A + 10 mg/kg citrinin). This damage was limited to the proximal tubular cells in dogs given only ochratoxin A (0.1 or 0.2 mg/kg). Myelin figures were in proximal epithelial cells of dogs given ochratoxin A alone or combined with citrinin. There was cytoplasmic disarray in dogs of all groups except for dogs given 5 mg/kg citrinin. This lesions was usually limited to the proximal tubules. The lesions, however, was found in cells of the distal tubules of dogs given 10 mg/kg citrinin alone. 相似文献