Kapillarkonvolute an der Pleura parietalis der Ziege (Capra aegagrus hircus)

The aim of the present study was to describe the morphology and location of convoluted capillaries of the pleura in the goat. Seven adult male and female goats were (1) fixed by perfusion with formaldehyde or (2) perfused with Indian ink and postfixed in formaldehyde. The parietal pleura was studied systematically for the presence of convoluted capillaries; areas containing such formations were dissected out, counterstained and examined light microscopically. The convoluted capillaries occur (1) within the normal level of the vascular bed, or (2) in villous elevations. The presence of convoluted capillaries is discussed in correlation with the functional studies of Lang (1965).     

Amyloid angiopathy with cerebral hemorrhage and senile plaque in aged dogs

Amyloid angiopathy with cerebral hemorrhage and senile plaques was found in the brain of aged dogs. In all 9 cases examined, 13 to 19 years old, 6 males and 3 females, amyloid deposits were observed mostly in the wall of cerebral arterioles and capillaries showed hyaline degeneration. The accumulation of amyloid fibrils measuring about 10 nm in diameter was seen in the cerebral vessel wall by electron microscopy. The cerebral hemorrhage was observed in 6 of 9 dogs and 2 of them showed massive hemorrhage. The hemorrhagic foci were sometimes closely contact with the vessels involved in amyloid angiopathy. In addition, senile plaques being classified into 2 types were found in the cerebral cortex of 3 dogs. The first type was characterized by the accumulation of degenerative neurites and often contained granular argyrophilic material. The second type had a well-defined amyloid core with neuritic halo. Amyloid deposits were also found in or around intestinal vessel walls of 3 dogs. The amyloid deposited in the cerebral vessels, senile plaques and intestinal vessels showed characteristic green birefringence under the polarized light even after potassium permanganate treatment.     

Effects of changes in power setting of an ultrasonic aspirator on amount of damage to the cerebral cortex of healthy dogs

OBJECTIVE: To determine the minimal ultrasonic aspirator pressure necessary to damage the cerebral cortex of healthy dogs. ANIMALS: 9 mixed-breed dogs. PROCEDURE: The study comprised 2 parts. In part A, 6 dogs were euthanatized immediately prior to the experiment. In part B, 3 dogs were anesthetized for recording of physiologic variables. In both parts, craniectomy and durotomy were performed to bilaterally expose the lateral aspect of the cerebral cortex. An ultrasonic aspirator was placed in contact with various areas of the cerebral cortex, and aspirator power was altered (10, 20, 30, and 40%). Duration of contact at each power was 5 and 10 seconds. Subsequently, gross morphologic and histologic damage was assessed in the cortex. RESULTS: Gross observations for all dogs were similar. At 10% power, visible or histologic damage was not evident in the cortex. At 20% power, the cortex was slightly indented from contact with the hand piece; however, cortical disruption was not evident. Cortical disruption was initially detectable at 30% power in some dogs and was consistently evident at 40% power in both sets of dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasonic aspirator power of < 20% created minimal acute morphologic damage to the cortex. Power settings between 20 and 30% may superficially damage the cerebral cortex in healthy dogs, whereas 40% power consistently damages the cerebral cortex. Knowledge of the degree of damage to cerebral cortex caused by various amounts of power for ultrasonic aspirators will allow surgeons to avoid damaging normal brain tissues during surgery.     

阿替美唑对小型猪特异性麻醉剂诱导大鼠大脑皮质内Fos蛋白表达的影响

研究阿替美唑对小型猪特异性麻醉剂(XFM)麻醉下大鼠大脑皮质Fos蛋白表达的影响,探讨阿替美唑颉颃XFM催醒大鼠与大脑皮质c-fos基因的关系。将72只SD纯种大鼠随机分为XFM对照组、XFM+阿替美唑组、XFM+生理盐水组,每组又按采脑时间点分成4个亚组。采用蛋白质印迹法检测大脑皮质内Fos蛋白表达量。结果表明:XFM麻醉大鼠大脑皮质内Fos蛋白表达量逐渐增加,与给药后10min比较差异显著(P<0.01或P<0.05);XFM麻醉大鼠腹腔注射生理盐水,各时间点Fos蛋白表达量与对照组间比较无显著差异(P>0.05);阿替美唑注射后引起XFM麻醉大鼠大脑皮质Fos蛋白表达量减少,与XFM对照组比较差异显著(P<0.01或P<0.05)。结果提示,大脑皮质c-fos基因参与了阿替美唑颉颃XFM麻醉作用。阿替美唑抑制XFM诱导大鼠大脑皮质Fos蛋白表达,可能是阿替美唑催醒XFM麻醉大鼠的重要机理之一。     

慢性镉暴露对小鼠大脑皮质的毒性损伤作用

为探究慢性镉暴露对小鼠大脑皮质的毒性损伤作用,选取雌性BALB/c小鼠用0(对照组)、5和25 mg/L不同浓度氯化镉自由饮水染毒16个月建立慢性镉中毒模型,试验结束后剖检采集小鼠完整脑组织,测定脑系数;光学显微镜和透射电子显微镜观察大脑皮质病理组织学和超微结构变化;比色法检测大脑皮质中总超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-P_X)的活性和还原型谷胱甘肽(GSH)、丙二醛(MDA)的含量。结果显示:与对照组相比,镉处理组脑系数均显著降低(P<0.05);镉处理组大脑皮质细胞核深染、固缩,呈三角形或不规则形,线粒体嵴断裂、溶解,部分呈空泡变性;镉处理组大脑皮质中T-SOD活力极显著下降(P<0.01),CAT活力显著下降(P<0.05),MDA、GSH含量极显著升高(P<0.01),5 mg/L氯化镉组GSH-PX活力显著升高(P<0.05),25 mg/L氯化镉组GSH-PX活力极显著升高(P<0.01)。提示:慢性镉暴露可影响小鼠脑发育,引起小鼠大脑皮质病理损伤、超微结构损伤和氧化损伤。     

苦马豆素诱导新生SD大鼠大脑皮质神经细胞凋亡

为阐明苦马豆素（SW）对新生SD大鼠大脑皮质神经细胞凋亡的影响,利用新生SD大鼠大脑皮质神经细胞体外原代培养模型,采用倒置相差显微镜、扫描电子显微镜及荧光显微镜观察sw对神经细胞的形态学损伤,运用流式细胞仪检测神经细胞凋亡率。结果显示,与对照组比较,各试验组神经细胞密度降低,神经网络减少且部分断裂;细胞表面粗糙,可见大量突起的小泡;细胞核出现浓缩、碎裂及新月形变化;随攻毒剂量的增加,神经细胞凋亡率呈明显上升趋势,与对照组相比,差异显著（P〈0．05）。结果表明,Sw能诱导新生sD大鼠大脑皮质神经细胞发生凋亡,这可能是Sw导致动物神经毒性损伤的作用机制之一。     

褪黑素对镉致鸭大脑皮质毒性损伤的保护作用

为探究褪黑素对镉致鸭大脑皮质毒性损伤的保护作用,本试验将16只20日龄高邮鸭随机分为4组,分别为对照组、褪黑素组、镉组、镉与褪黑素共处理组。对照组鸭自由采食饮水;褪黑素组鸭自由饮用含有0.2 mg·L^-1褪黑素的水;镉组鸭自由采食拌有2 mg·kg^-1氯化镉的饲料;镉与褪黑素共处理组鸭自由饮用含有0.2 mg·L^-1褪黑素水的同时自由采食拌有2 mg·kg^-1氯化镉的饲料。60 d后,剖检并采集鸭大脑皮质。比色法检测大脑皮质中丙二醛（MDA）和总抗氧化能力（T-AOC）的水平,ELISA法检测肿瘤坏死因子（TNF-α）、白介素-1β（IL-1β）的含量,免疫组化染色观察Nrf2核转位,免疫印迹法检测Nrf2、HO-1的蛋白表达。结果显示,与对照组相比,镉组鸭大脑皮质发生明显Nrf2核转位,T-AOC水平极显著降低（P<0.01）,MDA、TNF-α、IL-1β含量和Nrf2、HO-1蛋白表达量极显著升高（P<0.01）;与镉组相比,镉与褪黑素共处理组鸭大脑皮质Nrf2核转位减少,T-AOC水平显著升高（P<0.05）,MDA、TNF-α、IL-1β含量和Nrf2、HO-1蛋白表达量显著或极显著降低（P<0.05或P<0.01）。综上,褪黑素对镉所致的鸭大脑皮质毒性损伤具有一定的保护作用。     

Fas对镉暴露致大鼠大脑皮质自噬体形成的影响

为探究死亡受体Fas在镉暴露致大鼠大脑皮质自噬体形成中的作用,将24只21日龄雄性SD大鼠随机分为4组,分别为对照组、镉组、镉与对照病毒共处理组、镉与Fas基因沉默病毒共处理组。试验期间,对照组大鼠自由饮用纯净水,病毒处理组大鼠于第1天以每只1.4×10¹¹vg的剂量通过尾静脉注射相应病毒,4周后镉染毒组大鼠自由饮用镉水(50 mg·L^-1),持续90 d。试验结束后,透射电镜观察大脑皮质中自噬体数量,Western blot检测大脑皮质细胞外信号调节激酶1/2(Erk1/2)、p-Erk1/2、自噬相关蛋白7(ATG7)、自噬相关基因(Beclin-1)、微管相关蛋白1轻链3(LC3)蛋白表达水平,免疫荧光染色检测LC3表达水平。结果显示,镉暴露增加大脑皮质中自噬体数量,极显著激活Erk1/2并上调ATG7、Beclin-1、LC3蛋白表达水平(P<0.01);Fas基因沉默抑制镉引起的自噬体数量增加,极显著抑制镉致Erk1/2激活及ATG7、Beclin-1、LC3蛋白表达水平升高(P<0.01)。结果表明,Fas通过激活Erk1/2参与镉致大鼠大脑皮质自噬体形成。     

急性非洲猪瘟脑损伤及NF-κB介导脑水肿形成机制研究

【目的】 在试验条件下研究非洲猪瘟病毒（African swine fever virus，ASFV）所致急性脑损伤及核因子κB （NF-κB）介导脑水肿发生的相关病理机制。【方法】 18头健康长白猪随机分为2组，攻毒组（13头）和对照组（5头），攻毒组肌内注射剂量为10²HAD₅₀/mL （HAD₅₀：半数红细胞吸附量）的ASFV毒株Pig/HLJ/18，对照组注射等体积生理盐水，试验期为15 d。试验期间观察临床症状，剖检死亡猪并观察脑部病变；利用原位PCR检测进行病毒定位；HE染色及甲苯胺蓝染色观察脑组织病理变化；免疫组化染色法检测脑组织中肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、干扰素-γ（IFN-γ）、NF-κB、基质金属蛋白酶9（MMP-9）、水通道蛋白4（AQP-4）的表达。【结果】 攻毒组9头猪表现出临床神经症状，脑部剖检病变主要为脑膜充血和不同程度的脑实质水肿；ASFV主要位于脑部微血管中；病变早期主要为脑水肿，脑皮质区结构疏松、血管周围间隙增宽、神经元肿胀变圆、染色变淡，中后期除了表现脑水肿的特征外，还可见脑血管充血、多量微血栓形成及淋巴细胞浸润；免疫组化结果显示，攻毒组TNF-α、IL-1β、IFN-γ、NF-κB及MMP-9主要在神经元及胶质细胞中表达，AQP-4的阳性细胞主要是微血管周围的星形胶质细胞，与对照组相比，攻毒组上述6种因子的阳性表达率均极显著增高（P<0.01）。【结论】 急性非洲猪瘟脑损伤的主要表现为脑膜血管充血出血和脑实质水肿、组织学病变显示病毒性脑炎，ASFV感染脑部，促进炎性因子的异常高表达，通过激活NF-κB信号通路对TNF-α、IL-1β、IFN-γ的转录进行调控，使这几种炎性因子的产生和释放增多，扩大炎症反应，影响血脑屏障的通透性，还能上调MMP-9与AQP-4的表达，破坏血脑屏障，促进脑水肿的发生发展。     

Die Mikroangioarchitektur der Mukosa des Antrum pyloricum des Magens beim Kaninchen 1

Microangioarchitecture of the mucosa of the Antrum pyloricum in rabbit was studied by optical and scanning electron microscopy. Passing the lamina muscularis mucosae, arteries of the submucosa reach the lamina propria and branch in to the terminal arteries forming a subglandular network. From these vessels, two capillary nets arise. The first forms a capillary skein around the base of the glands, while the second ascends along the tubuli, moving upwards to the surface along the glandular tubuli. These ascending capillaries also arise directly from the subglandular arterioles of the lamina propria, as well as from capillaries of the basal parts of the glandular tubuli. Subepithelial capillaries form arcuate loops with 2-3 venules or collecting venules, which run into the venous net in the basal region of the lamina propria. Numerous horizontal interconnections exist between the collecting venules but arteriovenous anastomosis in the mucosa was not observed.     

Complementary distributions of amyloid-beta and neprilysin in the brains of dogs and cats

Neprilysin is an amyloid-beta-degrading enzyme localized in the brain parenchyma. The involvement of neprilysin in the pathogenesis of Alzheimer's disease has recently received much attention. We examined the localization of neprilysin and amyloid-beta, as well as the activity of neprilysin, in the brains of dogs and cats of various ages to clarify the relationship between neprilysin activity and amyloid-beta deposition. The distribution of neprilysin was almost identical in dogs and cats, being high in the striatum, globus pallidus, and substantia nigra, but very low in the cerebral cortex. The white matter and hippocampus were negative. Neprilysin activity in the brain regions in dogs and cats was ranked from high to low as follows: thalamus/striatum > cerebral cortex > hippocampus > white matter. Amyloid-beta deposition was first detected at 7 and 10 years of age in dogs and cats, respectively, and both the quantity and frequency of deposition increased with age. In both species, amyloid-beta deposition appeared in the cerebral cortex and the hippocampus. In summary, the localization of neprilysin and neprilysin activity, and that of amyloid-beta, were complementary in the brains of dogs and cats.     

Increased expression of vascular endothelial growth factor in neo-vascularized canine brain tissue

This retrospective study was done to characterize the levels of vascular endothelial growth factor (VEGF) and hypoxia inducible factor 1 (HIF-1α) in dog brains with neo-vascularization in the cerebral cortex of frontal, temporal, and parietal lobe by using immunohistochemistry (IHC) and Western blot. In neo-vascularized (NV) brains, we analyzed the number and area of blood vessels and the expression of VEGF and HIF-1α. The IHC results showed that the number and area of blood vessels, as assessed by immunolabeling for von Willebrand factor, was higher in the NV brain than in the control brain. The Western blot results showed that the level of VEGF was increased, predominantly in NV brain of the cerebral cortex relative to the clinically normal cerebral cortex, whereas the expression of HIF-1α in NV brains was not different from the control brains. Our study showed that dilatation of vessels and development of new vessels in the cerebral cortex were observed in cases of canine CNS disease and found increased expression of VEGF in canine brains with neo-vascularization.     

The activity and properties of adenosine triphosphatase in various swine organs (liver, cerebral and kidney cortex, small intestinal mucosa)]

Studies into the activity of adenosine triphosphatase (ATPase) in homogenates of liver, cerebral cortex, renal cortex, and mucosa of small intestine of swine have shown differentiated activity patterns, with peak activity developing in the liver. This has been related to a particularly high metabolism performance of the liver in fattening pigs. No difference was found to exist between magnesium activation of ATPase of swine tissue homogenates and that in tissue obtained from ruminants. ATPase which could be activated by sodium and potassium ions and inhibited by ouabain was detectable from cerebral and renal cortex. Sodium and potassium ATPases accounts from some 25 per cent of the total activity. ATPase that could be stimulated by calcium ions was recorded only from liver homogenate. The optimum pH values of ATPase were between 7.5 and 8 in the liver, 9 in mucosa of small intestine, and 9.5 in cerebral and renal cortex.     

热应激死亡鸡病理变化观察

对自然热应激和实验性热休克死亡鸡的病理学观察表明，其一致性的变化为肺充血、出血，呼吸毛细管与肺房结构损伤，肺气－血屏障有明显超微结构破坏；脑膜血管充血，神经细胞肿胀变性，延脑神经原细胞器肿胀、融解、变性；肾上腺皮质与髓质细胞超微结构变性、坏死，髓质细胞明显脱颗粒；卵泡膜和输卵管粘膜充血；肝淤血。肺与延脑神经细胞病变为热休克直接死因─—呼吸衰竭的结构基础；肾上腺细胞的病变是急性热休克肾上腺功能衰竭的结构基础。     

Acetylcholinesterase activity in specific regions of rabbit brain: Effect of pentobarbitone anesthesia

Acetylcholinesterase activity was determined in the cerebral cortex, cerebellum, hypothalamus, midbrain and medulla oblongata of a) control mature male rabbits, and b) male rabbits injected i.p. with an anesthetic dose of sodium pentobarbitone (60 mg/kg b.w.). Enzyme activity was highest in the midbrain and lowest in the cerebral cortex in controls. Pentobarbitone anesthesia increased enzyme activity in the cerebral cortex. No significant change in acetylcholinesterase activity occurred in the other brain areas studied following pentobarbitone administration. These findings are compared with the results of previous studies in the rat.     

IMAGING DIAGNOSIS—POLIOENCEPHALOMALACIA IN A CALF

A 2-month-old mix-breed calf developed acute blindness and ataxia. Serum thiamine concentration was deficient. In antemortem magnetic resonance imaging there were laminar T2-hyperintense regions extending along the cerebral cortex that primarily affected the gray matter. The lesions were relatively symmetric between the left and right hemispheres but no abnormalities were present at the frontal lobes. At necropsy, laminar autofluorescence of the cerebral cortex was observed under ultraviolet exposure at 365 nm, consistent with a diagnosis of polioencephalomalacia. Polioencephalomalacia in the bovine species is compared with that in other species, namely humans, dogs, and cats.     

疑核在大脑皮层参与免疫过程中的作用

实验用3～4月龄2.1～2.3kg健康青紫蓝家兔20只。麻醉后,5只刺激左侧大脑皮层,5只刺激右侧大脑皮层,10只损毁疑核后,刺激左侧大脑皮层。刺激前及刺激后不同时间采取血样,检测外周血T细胞百分率和PHA诱导的淋巴细胞转化率。结果:刺激左侧大脑皮层后,所测指标明显上升(P<0.01);而刺激右侧大脑皮层则无显著变化(P>0.05);损毁疑核后,刺激左侧大脑皮层时,所测T细胞百分率和PHA诱导的淋巴细胞转化率均无显著变化(P>0.05)。由此证明,左、右侧大脑皮层对细胞免疫具有分区调整现象,疑核可能是大脑皮层调整细胞免疫的中继站。     

Elektronenoptische Untersuchungen über Transsudationsvorgänge zwischen Blut- und Lymphkapillaren im Lymphobulbus des Kopulationsorganes beim Haushahn (Gallus domesticus)

Electronmicroscopical studies of transudation between blood capillaries and lymph capillaries in the lymphobulbus of the phallus of the cockerel (Gallus domesticus) The blood capillaries of the lymphobulbus cloacae may be divided into circulatory and transudation capillaries and may be distinguished from one another and from the lymph capillaries by ten criteria. The specific structure of the wall of these capillaries permits transudation of lymph from the blood-vascular to the lymphatic system. The lymph passes through the pores and fenestrae of the transudation capillaries into the interstitium and from here by two routes into the lymphobulbus. One route is intracellular-vesicular, and the other is intercellular (between the endothelial cells of the lymph capillaries). The contraction of the striated M. sphincter cloacae during erection of the phallus presses the lymph through the ductus lymphaticus bulbospongiosus cloacae into the corpus cavernosum of the phallus. There is a relationship between the structure and functional stages of the lymphobulbus and age, and between the former and the levels of the steroid sex hormones.     

出生前山羊大脑皮质的形成和发育

对山羊胚胎大脑皮质形成及其神经元发育的形态学变化进行了研究，结果表明：（1）山羊胚胎不同类型大脑皮质的皮质板形成时间顺序为旧皮质、新皮质→海马皮质，与种系发生规律相反，提示神经系统内部结构的形成并非完全符合种系进化，而与动物个体组织结构自身的发展相关。不同类型大脑皮质皮质板的分化顺序为古皮质→旧皮质→新皮质，与种系发生的顺序相符。（2）山羊胚胎海马皮质锥体细胞的发育较早，按由深到浅的次序发育，而海马皮质中的非锥体细胞于第19周开始发育。梨状叶皮质锥体细胞发育的较早，最先出现在深层，颗粒层第18周出现。大脑新皮质各层神经元发育顺序依次为：内锥体层→外锥体层、多形层→内颗粒层→外颗粒层。各种类型皮质的神经元在出生前都未发育成熟。     

Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical and histopathological findings

The aim of the present study was to assess the clinical and histopathological findings in a canine model of ischemic stroke. Cerebral ischemic stroke was induced by middle cerebral artery occlusion in four healthy beagle dogs using silicone plugs. They showed neurological signs of forebrain dysfunction such as reduced responsiveness, head turning, circling, postural reaction deficits, perceptual deficits, and hemianopsia. These signs gradually regressed within 4 weeks without therapy. On magnetic resonance imaging, T2 hyperintensity and T1 hypointensity were found in the cerebral cortex and basal ganglia. These lesions were well-defined and sharply demarcated from adjacent brain parenchyma with a homogenous appearance. No abnormalities of the cerebrospinal fluid were observed. At necropsy, atrophic and necrotic lesions were observed in the cerebral cortex. The cerebral cortex, basal ganglia, and thalamus were partially unstained with triphenyl-tetrazolium chloride. Histopathologically, typical features of infarction were identified in cortical and thalamic lesions. This study demonstrates that our canine model resembles the conditions of real stroke patients.