Microvasculature of bone

The three dimensional vascular microarchitecture of mercox resin on the lateral surface of parietal bone in Wistar strain adult male rats (b. w. 260–350 g.) was studied in relation to bone formation by SEM observation of corrosion casts. The microarchitecture was a single layer of network composed of precapillary artery, capillary and postcapillary vein, which were serpigious, sometimes joined with the vein from the vascular foramen of bone. The meshes of this network, which were irregular and varied in size, existed apart from the bone surface. According to the report of Iwaku and Ozawa (1986), it was reported that the vascular microarchitecture of the bone surface was very changable during the process of bone remodeling and this network, which was shown on the flat bone surface in this study, was very similar to one in the resting phase and/or the period in which the bone formation further advanced. From these facts and the morphological features of the bone surface observed here by SEM, it is suggested that this vascular network was closely related with the resting stage and/or the period in which bone formation further advanced in bone remodeling.     

80例健康青年分别经针刺或艾灸肺俞穴后的肺功能变化

目的：探讨针刺与艾灸肺俞穴对健康人肺功能的影响。方法：我们选择了20－22岁健康男性80例，随机分为针刺组和艾灸组各40例，于针刺，艾灸前和针刺，艾灸后10min测试用力肺活量（FVC），用力呼气量（FEV1．0），最大呼气中段流速（MMF），最大呼气流量（PEFR），75％，50％，25％肺活量时的最大呼气流速（V75，V50，V25），结果：显示经针刺和艾灸肺俞穴后2组FVC，FFV1．0均显著增加，P＜0．05，2组间比较针刺组FVC明显高于艾灸组，P＜0．05，而且艾灸组MMF，V25亦显著降低P＜0．05，结论：健康人经针刺和艾灸肺俞穴后均可使大气道阻力减少，肺容量增加，提示一定量的艾燃烧后的烟雾可使健康人肺功能受到影响，使肺的小气道收缩，出现阻塞性改变。     

前列腺素E1和一氧化氮联合治疗室间隔缺损并肺动脉高压的疗效观察

目的 :观察静脉应用前列腺素E1(PGE1)、吸入一氧化氮 (NO)及二者小剂量联合应用对室间隔缺损 (VSD)并肺动脉高压的治疗作用。方法 :将 2 4例VSD并肺动脉高压的病人随机分为 3组 ,观察静脉注射PGE16 0ng/ (kg·min)、吸入NO 2 0ppm及静脉注射PGE130ng/ (kg·min)联合吸入NO 10 ppm对病人的血流动力学及血氧饱合度的影响。结果 :静脉注射PGE16 0ng/ (kg·min)使肺动脉平均压 (MPAP)明显下降 ,体动脉平均压 (MSAP)亦有所下降 ,心指数 (CI)明显增加。吸入NO 2 0 ppm组MPAP明显下降而MSAP无明显变化 ,CI有所升高 ,但差别不显著。静脉注射PGE130ng/ (kg·min)同时吸入NO 10 ppm组MPAP明显下降 ,但不显著 ,CI明显升高。 3组血氧饱合度均明显升高。结论 :联合应用小剂量PGE1和NO不仅能有效降低MPAP ,又能适当轻度降低MSAP ,改善心功能 ,减轻了NO的毒副作用 ,是一种较理想的治疗方案     

Revisit on congenital bronchopulmonary vascular malformations: a haphazard branching theory of malinosculations and its clinical classification and implication.

We propose a haphazard branching theory to support the concept of bronchopulmonary malinosculations, and we apply this theory to classify congenital bronchopulmonary vascular malformation (BPVM) based on the anatomical results we have found. Between January 1990 and December 1997, a total of 22 pediatric patients (10 male and 12 female), aged 2 days to 14 years (median, 19.6 months), with congenital BPVM were enrolled in this retrospective study. Study modalities include the clinical features and plain chest films (n = 22) plus at least two of the following: echocardiography (n = 13), barium esophagraphy (n = 2), bronchoscopy (n = 4), contrast bronchography (n = 8), high-resolution direct coronal CT (n = 1) and electron beam or ultrafast CT (n = 1) of the chest, MRI (n = 10), MRA (n = 1), contrast cineangiocardiography (n = 9), surgery (n = 11), or autopsy (n = 2). The salient clinical features were recurrent lung infections in 14 patients, acute respiratory distress in 13, associated cardiovascular malformations in 8, dextroversion in 7, congestive heart failure in 7, dextrocardia in 4, and complex congenital heart diseases in 4. There were abnormal openings (malinosculations) of the pulmonary airway in 20 patients: to an artery in 12, to a vein in 8, and to the lung parenchyma in 9. These 22 patients with congenital BPVM can be classified into bronchial malinosculation (10 cases), arterial malinosculation (2 cases), and bronchoarterial malinosculation (10 cases). Congenital BPVM can be classified in terms of bronchopulmonary malinosculation based upon a haphazard branching theory, in which abnormal communications between two independent systems (primitive foregut system and aortic-pulmonary arch system) occurred coincidentally rather than causally.     

哮喘患儿血清嗜酸性粒细胞阳离子蛋白改变及其意义

目的：评价变应性哮喘患儿血清嗜酸性粒细胞阳离子蛋白（S-ECP）水平改变及其意义。方法：测定25例哮喘发作期患儿糖皮质激素吸入治疗12周前后，及20例未予糖皮质激素吸入治疗的哮喘缓解期患儿S-ECP水平，并对发作期患儿S-ECP水平变化与血嗜酸性粒细胞计数（B-EOS）、肺功能一秒用力呼气量（FEV1）、一秒用力呼气量比用力肺活量（FEV1/FVC）及症状评分的关系作相关性分析。结果：哮喘发作组治疗后S-ECP水平较治疗前显著降低，与对照组（健康儿童10名）比较差异无显著性；哮喘缓解组S-ECP水平明显高于发作组治疗后，但明显低于发作组治疗前。哮喘发作组治疗前S-ECP水平变化与B-EOS无相关性，与FEV1、FEV1/FVC呈负相关，与症状评分呈正相关。结论：监测S-ECP水平可作为评价哮喘气道炎症程度、病情预后和指导抗炎治疗的有效指标。     

肾小球微血管构型的扫描电子显微镜观察

应用微血管铸型扫描电镜技术研究8例成人肾脏的肾小球微血管构筑,结果发现:1.输入小动脉在肾小球血管极处分为2～5支小球内小叶微动脉。输入小动脉血管铸型的直径为126.35±20.5μm。2.肾小球是由小球内小叶微动脉、毛细血管、毛细血管网小叶间交通支和毛细血管输出根所构成的近似于球状体,小球内每个毛细血管网小叶均是一个独立的机能解剖学单位;3.299个肾小球均有一支输出小动脉,只有一个肾小球有两支输出小动脉。输出小动脉的血管铸型直径为91.35±11.7μm。4.输出小动脉起始处具有毛细血管前括约肌装置,此结构在调控肾小球内的微循环血流有着重要意义。     

自体大隐静脉移植治疗周围血管损伤22例分析

目的：探讨周围血管损伤自全大隐静脉移植治疗的方法。适应证和治疗效果。方法：回顾性分析22例周围血管损伤自体大隐静脉移植治疗的临床资料，并阐述了术中注意事项，提出最佳手术时机及预后情况。结果：22例均采用自体大隐静脉移植，痊愈19例（86.4%)。截肢3例（13.6%），22例患者无死亡，随访2-9年，20例肢体功能恢复满意，2例移植段狭窄，但肢体功能良好。结论：自体大隐静脉移植是治疗周围血管损伤行之有效的方法之一。血管吻合的时间应在24h以内，最佳为8h以内。     

肺心病患者血清碱性成纤维细胞生长因子水平的变化及其与肺动脉压的关系

目的　探讨碱性成纤维细胞生长因子 (b FGF)在低氧性肺动脉高压发病中的作用。方法　采用酶联免疫吸附法对具有低氧性肺动脉高压的肺心病患者 2 1例、无低氧性肺动脉高压的慢性阻塞性肺疾病 (COPD)患者 2 3例和 2 4例正常人血清 b FGF水平进行检测 ,以多普勒超声心动仪测定肺心病和 COPD患者的平均肺动脉压 (m PAP)。结果　肺心病组 m PAP水平 (33.33± 7.0 3m m Hg)明显高于 COPD组 (13.13± 2 .34mm Hg) ,P<0 .0 0 1;肺心病组血清 b FGF水平 (6 9.84± 16 .2 9pg/m l)明显高于 COPD组 (43.94± 7.5 7pg/ml)和正常对照组(44 .6 4± 6 .31pg/m l) ,P<0 .0 0 1;肺心病血清 b FGF水平与 m PAP之间呈明显正相关 ,r=0 .730 ,P<0 .0 0 1。结论慢性肺心病患者血清 b FGF水平明显升高 ,可能与其慢性低氧性肺动脉高压的形成有一定的关系。     

儿童髓母细胞瘤中VEGFR-2的表达

目的：探讨血管内皮生长因子受体VEGFR－2在儿童髓母细胞瘤中的表达及临床意义。方法：采用免疫组化LSAB法检测84例获随访的儿童髓母细胞瘤中的VEGFR－2表达，按术后生存期3，5，10年分为A，B，C三组，使用Cox回归统计分析。结果：84例儿童髓母细胞瘤中，VEGFR－2阳性表达74例（88．09％），A，B，C三组间VEGFR－2阳性表达分别为100％，88．89％，55．33％（P＜0．01），Cox回归分析显示VEGFR－2是影响生存时间的一个独立的预后因子，它与预后存在负相关关系。结论：VEGFR－2表达水平可作为儿童髓母细胞瘤的预后指标之一。     

烹调油烟致大小鼠肺癌的实验研究

[目的]了解烹调油烟（cooking oil fumes，COF）的动物致癌性。[方法]采用动式染毒法给Balb／c小鼠（雌雄各半）吸入COF浓度为9．09、20．65、38．85mg／m^3，染毒1次／1～2d，30min／次，共150次，计8个月；SD大鼠（雌雄各半）吸入COF浓度为6、88、15．06、35．33mg／m^3，染毒1次／2d，30min／次，共191次，计12．5个月。分别制备COF慢性中毒动物模型；两实验均设空白对照组，吸入与实验组相同温度的清洁空气。[结果]COF诱发Balb／c小鼠实验组肺癌总发生率为18、95％（29／153），低、中、高浓度组肺癌发生率分别为15．09％、20、00％和22．00％，与对照组差异均有显著性。但低、中、高三组间差异无显著性（P〉0．05）；COF诱发SD大鼠肺癌总发生率为9、10％（9／99），低、中、高浓度组肺癌发生率分别为6．45％、8．57％、12．12％，高浓度组肺癌发生率高于对照组（P〈0．05）。各性别组间肺癌发生率的差别无显著性（P〉0．05）。[结论]COF可以诱导Balb／c小鼠和SD大鼠肺癌，诱发的肺癌主要为肺腺癌（小鼠28／29，大鼠7／9），余为小细胞肺癌。