模拟失重大鼠后肢血管适应性变化的形态学研究

模拟失重大鼠后肢血管适应性变化的形态学研究毛秦雯张远强张立藩（第四军医大学组织学与胚胎学教研室）本研究的目的在于采用形态学方法观察模拟失重大鼠后肢血管的适应性变化，以对失重引起的立位耐力降低的机制提供新的理论依据。动物分对照（Ｃｏｎｔ）、悬吊４周（Ｓ...     

兔蛛网膜下腔出血后海马CA_1区微血管形态定量研究及尼莫通的干预作用

目的定量研究兔蛛网膜下腔出血(SAH)后海马CA 1 区微血管形态学变化及相应的神经元病理改变 ,并观察尼莫通 (ND)的治疗作用。方法采用枕大池两次注血法制作兔SAH模型 ,运用内源性过氧化物酶法显示兔SAH后5d海马CA 1 区微血管 ,用体视学方法对脑微血管进行定量分析 ,并观察了海马CA1 区组织病理学变化。结果SAH后海马CA 1 区微血管除直径外 ,体积密度、长度密度、表面积密度较正常组均有明显下降 (P<0 .01) ,且存在神经元的变性坏死 ;ND治疗后海马CA 1 区微血管密度恢复正常 ,与SAH组比较有显著性差异 ,神经元数量显著增加 (P<0.01)。结论SAH后微循环障碍是继发性脑损伤的病理学基础 ;ND具有改善微循环 ,保护神经元的作用。     

兔蛛网膜下腔出血后海马CA1区微血管形态定量研究及尼莫通的干预作用

目的 定量研究兔蛛网膜下腔出血（SAH）后海马CA1区微血管形态学变化及相应的神经元病理改变,并观察尼莫通（ND）的治疗作用。方法 采用枕大池两次注血法制作兔SAH模型,运用内源性过氧化物酶法显示兔SAH后5d海马CA1区微血管,用体视学方法对脑微血管进行定量分析,并观察了海马CA1区组织病理学变化。结果 SAH后海马CA1区微血管除直径外,体积密度、长度密度、表面积密度较正常组均有明显下降（P＜0．01）,且存在神经元的变性坏死;ND治疗后海马CA1区微血管密度恢复正常,与SAH组比较有显著性差异,神经元数量显著增加（P＜0．01）。结论 SAH后微循环障碍是继发性脑损伤的病理学基础;ND具有改善微循环,保护神经元的作用。     

小鼠及人正常组织谷胱甘肽－S－转移酶π基因与三种癌基因的分布和相互关系的研究

用Ｈａｂｉｇ改良法测定人及ＤＡＢ小鼠正常组织中谷胱甘肽－Ｓ－转移酶活性及π基因与３种癌基因的分布。人７种正常组织中ＧＳＴπＲＮＡ相对含量为４．８６～０．２５，以胎盘最高，其次为膀胱、肺、胃。小鼠的ＧＳＴ活性为１７．７～１２．４７，肝最高，其次为胃、肺和肾。ＧＳＴπＲＮＡ为１．９８～０．４２５，以胃最高，脾和肺次之，ＧＳＴ活性与ＧＳＴπＲＮＡ的检测结果基本一致。人７种正常组织中，Ｎ－ｒａｓ的相对含量为２０～２．９４，以胎盘含量最高，直肠、乳腺次之。Ｃ－ｍｙｃ为２３．４～７．３８，胎盘、肺、膀胱较高。ｖ－ｅｒｂ－Ｂ为９．０５～０．３８，以胎盘最高，直肠、胃次之。在小鼠６种组织中，Ｎ－ｒａｓ的基因相对含量为６．２３～１．０４，以肺、脾较高，胃、肝、心、肾次之。Ｃ－ｍｙｃ为１３．７６～５．３１，肺、胃较高。ｖ－ｅｒｂ－Ｂ为８．７２～２．０９，肺、胃较高，脾次之。说明ＧＳＴπ对肿瘤的发生有一定的制约作用。     

常压缺氧大鼠血浆和肺组织TXB_2和6－keto－PGF_（1α）的动态变化

本文观察常压缺氧２４ｈ及１，２，４ｗ（６ｈ／ｄ，６ｄ／ｗ）后大鼠血小板数及聚集率和血浆及肺ＴＸＢ＿２和６－ｋｅｔｏ－ＰＧＦ＿（１α）的动态变化。结果表明（１）缺氧大鼠血小板数呈先增加、后恢复、再下降，血小板聚集率呈先减少、后增加再减少的动态变化。（２）血浆ＴＸＢ＿２和６－ｋｅｔｏ－ＰＧＦ＿（１α）均明显升高，（３）肺组织６－ｋｅｔｏ－ＰＧＦ＿（１α）升高早于ＴＸＢ＿２，提示ＰＧＩ＿２参干旱期缺氧肺血管张力调节。（４）缺氧大鼠２周时肺动脉高压达到高峰，右心室明显肥厚，而肺组织ＴＸＢ＿２至缺氧４周后才见增加，表明ＴＸＢ＿２不是缺氧早期肺血管收缩的主要因素。     

常压缺氧大鼠血浆和肺组织TXB2和6—keto—PGF1α的动态变化

本文观察常压缺氧２４ｈ及１，２，４ｗ后大鼠血小板数及聚集率和血浆及肺ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α的动态变化。结果表明（１）缺氧大鼠血小板数呈先增加、后恢复、再下降，血小板聚集率呈先减少、后增加再减少的动态变化。（２）血浆ＴＸＢ２和６－ｋｅｔｏ－ＰＧＦ１α均明显升高。（３）肺组织６－ｋｅｔｏ－ＰＧＦ１α升高早于ＴＸＢ２，提示ＰＧＩ２参于早期缺氧肺血管张力调节。（４）缺氧大鼠２周时肺动脉高压达到     

血管内皮生长因子在尾悬吊模拟失重大鼠肺组织中表达的研究

目的：研究尾悬吊模拟失重大鼠肺组织血管内皮生长因子的变化。方法：采用尾悬吊模拟失重，分为悬吊7 d和21 d及相应对照4组，每组10只健康雄性SD大鼠，共40只大鼠。并采用免疫组织化学技术检测肺组织的血管内皮生长因子表达情况。结果：7 d尾悬吊模拟失重大鼠肺组织血管内皮生长因子的表达水平明显高于正常对照组（P<0.05），且21 d悬吊组模拟失重大鼠肺组织血管内皮生长因子的表达水平仍较高（P<0.05），但增高程度已明显低于7 d悬吊组。结论：在模拟失重条件下肺组织血管内皮生长因子的表达水平增高，并且随着时间延长增高程度会有所降低.     

NO抑制剂导致大鼠多脏器损伤的形态学研究

本文观察了ＮＯ抑制剂对小肠、脑、心、肺、脾、肝、肾、肾上腺、胸腺的形态学改变，结果表明，单用ＬＰＳ或ＮＡＭＥ１ｈ内均未见脏器明显病理改变，但ＬＰＳ＋Ｌ一ＮＡＭＥ１ｈ后，即可引起肠管紫绀，肠腔大量出血；组织学检查，小肠、肺呈弥慢性出血，肾、脾呈梗塞性坏死，但心、肝变化不明显。延长观察时间，单独注射Ｌ一ＮＡＭＥ２ｈ，小肠绒毛毛细血管明显充血扩张，６ｈ后可见绒毛内毛细血管内皮损伤，局部出血。但Ｄ一ＮＡＭＥ并不引起同样病变。本研究表明，ＮＯ释放对维持内皮细胞在病理或正常条件下的完整性具有重要意义。     

兔胸腹部爆炸伤后不同器官微血管通透性的变化

目的探讨爆炸性冲击伤后不同组织器官微血管通透性变化的特点及其可能的机理。方法采用雷管对兔的爆炸性冲击损伤模型 ,以及 125I-白蛋白标记的方法 ,观察爆炸性冲击波对兔心、脑、肺、肾、肝组织中的微血管通透性的影响。结果距爆源20cm处的爆炸冲击波平均压力峰值为174 .4kPa,可引起红细胞压积增加为14.9 % (与对照组相比 ) ,血浆丢失为对照的5.12倍 ;距爆源10cm时 ,爆炸冲击波的压力峰值可陡增至1000kPa以上 ,所致白蛋白漏出率为伤前的1.5倍 ,心、脑、肺、肾组织中的残留放射性较对照组增加约1 .6～1.9倍。结论爆炸冲击波能引起红细胞压积明显增加 ,血浆丢失 ,以及心、脑、肺、肾组织中微血管通透性的增加。     

心肌缺血／再灌注对球结膜微循环的影响以及一氧化氮的调节作用

对照观察兔急性心肌缺血／再灌注时球结膜微循环的变化，测定动物血浆中内皮舒张因子／一氧化氮（ＥＤＲＦ／ＮＯ）、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１α（６－Ｋｅｔｏ－ＰＧＦ１α）、超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）的浓度变化，并用光镜和电镜对缺血／再灌注心肌组织作形态学观察。结果发现：（１）兔心肌缺血／再灌注后球结膜微循环异常；表现为Ａ３、Ａ４微动脉血管管径缩小，毛细血管交换距离增大。（２）血浆中ＥＤＲＦ／ＮＯ水平降低；（３）血浆ＴＸＢ２、ＭＤＡ水平升高，ＳＯＤ、６－Ｋｅｔｏ－ＰＧＦ１α下降；（４）光镜下：缺血区心肌组织细胞肿胀变性。电镜下：内皮细胞肿胀，部分毛细血管腔内有红细胞、白细胞附壁阻塞，线粒体肿胀，糖原颗粒减少。结果提示：心肌在较短时间缺血后再灌注（缺血３０ｍｉｎ再灌注３０ｍｉｎ）后就可产生组织损伤，这可能与血管内皮受损，ＥＤＲＦ／ＮＯ合成释放减少，缩血管物质ＴＸＡ２升高，血小板、白细胞粘附、聚集在血管内皮上，氧自由基产生过多等有关。上述因素共同作用导致缺血／再灌注心肌微循环功能障碍进而引起组织形态改变。     

模拟失重时兔血液中血管内皮细胞数量的变化

模拟失重时兔血液中血管内皮细胞数量的变化沈羡云１陈建和１孟京瑞１董欣１王玉清１钱冠清２刘会齐２近几年来，国内外进行了循环内皮细胞数（ＣＥＣ）检测技术及其临床应用的研究［１，３］。研究结果表明，血液中ＣＥＣ的变化可以反映许多病理情况下血管内膜的损伤程度...     

The activity of lung irritant receptors during pneumothorax, hyperpnoea and pulmonary vascular congestion

1. The activity of lung irritant receptors during pneumothorax, hyperpnoea and pulmonary congestion has been studied by recording from single vagal nerve fibres from the receptors in rabbits.2. The receptors were stimulated during induction and during removal of pneumothorax.3. Pneumothorax caused a greater depression of minute volume in bilaterally vagotomized rabbits, compared with those with intact vagus nerves.4. Hyperpnoea due to breathing through an added dead space increased the discharge of the receptors. Experiments on paralysed and artificially ventilated rabbits showed that this was not a direct action of the asphyxial changes in blood gas tensions.5. Pulmonary congestion, induced by inflating a balloon in the left atrium, stimulated the receptors in paralysed artificially ventilated rabbits.6. The evidence that the receptors cause vagal reflex hyperpnoea and bronchoconstriction is discussed, together with their role in the reflex ventilatory and bronchomotor changes in the conditions studied.     

Reduced natriuresis during weightlessness

Summary The kidney response to weightlessness was measured in one volunteer during a 1-week space mission. Shortly after entering microgravity and later during the mission, consecutive urine sampling periods were monitored, covering in total about 50% of the inflight time. Preflight references were a sequence of ground-based experiments, which evaluated body fluid metabolism with different degrees of standardization. Additional variables, such as circadian rhythms and cortisol-associated stress, were also monitored. In contrast to current hypotheses, the volunteer showed a pronounced reduction in natriuresis and diuresis during the entire space flight, despite a considerable weight loss. For the first time, the urinary excretion of the renal natriuretic peptide urodilatin was also measured. Both, during the preflight experiments and during weightlessness, close correlations between urodilatin excretion and sodium excretion were observed. However, the correlation between natriuresis and urodilatin excretion was considerably altered during weightlessness. We conclude that the loss of body weight during space flight is not related to an increased renal fluid loss and that urodilatin might counteract the decrease in renal excretion observed in weightlessness.     

家兔急性肺栓塞对肺血管内皮细胞超微结构及血清一氧化氮含量的影响

目的 探讨急性肺栓塞（APE）对肺血管内皮细胞（PVECs）的结构及血清一氧化氮（NO）含量的影响。 方法 19只日本大耳兔,随机分成假手术组、栓塞2 h、4 h组(n=3)和8 h组（n=10）。通过输入自体血栓建立家兔急性肺栓塞模型后,采用HE染色光学显微镜下观察肺的病理组织学变化;透射电子显微镜下观察PVECs在肺栓塞2 h、4 h及8 h的超微结构变化;硝酸还原酶法测定相应时间点血清NO含 结果 HE染色显示栓塞组肺动脉内有血栓,肺间质炎性病变,肺淤血;透射电子显微镜显示,栓塞组PVECs水肿、破裂,线粒体肿胀,内质网空泡化,并随栓塞时间延长PVECs出现坏死脱落,细胞器溶解。肺栓塞2 h、4 h和8 h血清NO含量均低于栓塞前,与栓塞前比较差异有显著性意义（P＜0.05）。 结论 家兔APE可致PVECs超微结构改变和血清NO含量下降,且两者间关系密切。     

Cytopathologic observations of the lung of adult newts (Cynops pyrrhogaster) on-board the space shuttle, Columbia, during the Second International Microgravity Laboratory experiments

Four adult female Japanese newts, Cynops pyrrhogaster, were carried for 15 days aboard the orbiting space shuttle, Columbia, in July of 1994, as part of the Second International Microgravity Laboratory, IML-2 aquatic animal experiments. These previously fertilized newts, after stimulation with chorionic gonadotropin by a spaceflight adapted injection procedure, deposited numerous eggs for study of early development during weightlessness. The primitive saccular lungs of the two newts which survived the spaceflight revealed by TEM marked pulmonary cytopathologic changes including basal laminar separation, microvillar degeneration, and cytoplasmic granular changes in the primary granulated pneumocytes. Also, intracellular edema in the pulmonary collagenous matrix and vacuolar changes in the ciliated pulmonary lining cell type and in vascular endothelial cells were observed. These changes, triggered by the spaceflight, and not seen in controls also relying on respiration via the skin, may reflect a chronic mild hypoxia as it is known that newts undergoing oviposition are subject to increased oxygen demand.     

Lung injury via oxidative stress in mice induced by inhalation exposure to rocket kerosene

Rocket kerosene (RK) is a new rocket propellant. Toxicity occurs if a high level of RK is inhaled. To study the toxicity of RK in lung and the mechanisms of RK-induced lung jury, a total of 72 male ICR mice (1.5 months, adult) were randomly assigned to the RK exposure group (RKEG) and normal control group (NCG). Mice were whole-body exposed to room air or aerosol of 18000 mg/m³ RK for 4 hours. Histopathological analysis was performed to evaluate the pulmonary lesions. Oxidative stress was assessed by assay of MDA, SOD, GSH-PX and TAOC. Inflammatory response was estimated by detecting inflammatory cell counts, TNF-α and IL-6 protein levels in serum. The results showed that after 2 to 6 hours of RK exposure, pulmonary vascular dilatation, congestion and edematous widening of the alveolar septum were noted. After 12 to 24 hours post-exposure, diffuse hemorrhage in alveolar space were found, along with the progressive pulmonary vascular dilatation and edematous widening of alveolar septum. During 3 to 7 days of RK-exposure, inflammatory cells were scattered in the lung tissue. The pathological alterations of the lung were alleviated after 14 days post-exposure, and showed significant improvement after 21 days post-exposure. After 30 days of RK exposure, the pathological changes in the lung tissue were nearly recovered except the local thickening of the alveolar wall. Compared with NCG, RK inhalation produced a significant increase of MDA levels and a significant decrease of SOD, GSH-Px and TAOC activity in the lung after 2 hours post-exposure (P < 0.05). There were significant increases of TNF-α and IL-6 protein levels in serum of mice in RKEG after 2, 6 and 12 hours and 1, 4 and 7 days post-exposure compared with NCG (P < 0.05). TNF-α protein levels had a sharp increase after 4 days of exposure. IL-6 protein level was increased at early phase of experiment and then gradually decreased along with the prolonged course of exposure. Considering that the RK-induced lung injury was through the oxidative stress, inhibition of oxidative stress after RK exposure may be urgently needed.     

Characteristic of Changes in the Structure and Metabolism of the Vastus Lateralis Muscles in Monkeys after Space Flight

Monkeys subjected to space flight were found to have significant decreases in the sizes of slow and rapid fibers in the vastus lateralis muscle, due not only to weightlessness but also, to some extent, to restriction of movement activity within the capsule. The quantity of total protein in muscle fibers did not decrease. The respiratory peak in the pool of vastus lateralis muscle fibers decreased after space flight, as did the activity of oxidative enzymes (particularly in rapid fibers of the vastus lateralis muscle).     

模拟失重大鼠肺组织显微结构和一氧化氮合酶表达的动态变化

目的 观察模拟失重对大鼠肺组织显微结构及其一氧化氮合酶(NOS)表达的影响,为模拟失重时肺组织的适应机制研究积累资料.方法 采用Wistar雄性大鼠-30°尾部悬吊模拟失重生理效应.常规光镜和免疫组织化学方法 观察悬吊7 d组(TS7)、14 d组(TS14)及对照组(Con)肺组织显微结构和结构型NOS(cNOS)、诱导型NOS(iNOS)表达.结果 TS7组大鼠出现肺实变、肺水肿、支气管黏膜内淋巴细胞浸润、肺泡内有红细胞及肺泡融合.TS14组大鼠肺病变较TS7组大鼠明显加重,表现为肺泡融合增多、肺泡内更多红细胞和肺泡壁增厚.各组大鼠肺组织cNOS表达区域主要为支气管上皮细胞、血管内皮细胞和平滑肌细胞,各组间表达水平无统计学差异.iNOS表达在TS7、TS14组血管内皮细胞和平滑肌细胞表达显著增多,其中TS14组血管内皮细胞表达量高于TS7组.结论 模拟失重大鼠肺组织形态学变化可能与肺循环iNOS表达增加有关.     

Effect of artificial gravity in space flight on the content of water-soluble proteins in nerve tissue structures

The content of water-soluble proteins was investigated in the gray and white matter of the spinal cord, the spinal ganglia, and the sensomotor cortex of rats after a space flight lasting 18.5 days. The content of water-soluble proteins in the gray and white matter of the spinal cord and in the spinal ganglia of rats exposed to the action of weightlessness was significantly reduced after 4.5–9.5 h. In rats kept under conditions of artificial gravity during flight the content of water-soluble proteins was reduced in the white matter of the spinal cord. In animals kept previously under conditions of weightlessness 25 days after space flight a significant increase was found in the level of, water-soluble proteins in the gray matter of the spinal cord. In the gray matter of the sensomotor cortex of rats kept under conditions of weightlessness or of artificial gravity no changes were found (compared with controls kept in the ordinary animal house) in the content of water-soluble proteins whether 4.5–9.5 or 25 days after the satellite has landed.Institute for Medico-Biological Problems, Ministry of Health of the USSR, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 10, pp. 421–424, October, 1978.     

Contributory factors to orthostatic intolerance after simulated weightlessness.

Various factors may contribute to orthostatic intolerance (OI) observed after space flights or simulated weightlessness such as bed rest experiments: individual physical and physiological factors (arterial blood pressure (BP), height), physiological changes induced by real or simulated weightlessness (hypovolaemia, increase in venous distensibility), and space flight or simulation conditions (duration and counter-measure application). Our purpose was to test which of these factors were dominant in contributing to the OI. This was assessed in 47 healthy men participating in bed rest experiments of 4, 14, 28, 30 and 42 days, with or without counter-measures (medical stockings, lower-body negative pressure (LBNP), LBNP + muscular exercise). Nineteen subjects did not finish the orthostatic test (60 degrees head-up tilt or stand test) after bed rest. The occurrence of OI was associated with greater height, low resting BP, greater changes in resting lower-limb venous distensibility throughout the bed rest, and absence of counter-measures.