内毒素预处理对内毒素血症大鼠各器官细胞凋亡的作用

目的　观察大鼠内毒素血症时各脏器的细胞凋亡及内毒素 (LPS)预处理对其作用。方法　将雄性Wistar大鼠 42只随机分为 3组 :生理盐水组 (N组 ,n =6) ;LPS对照组 (L组 ,n =18) ;LPS预处理组 (P组 ,n =18) ,P组 :首次 ,经腹腔注射LPS 0 .2 5mg/kg体重 ;2 4h后再经腹腔注射LPS 0 .5 0mg/kg体重 ,其余两组在上述时间均给予等量生理盐水 (NS) ;第 2次腹腔注射 72h后 ,L组和P组经静脉注入LPS 10mg/kg体重 ,N组给予等量NS。在静注LPS后 ,N组取 6只在 6h末、L组和P组分别在静注 2、4、6h时各取 6只大鼠处死。取动物肺、肝、小肠、脾等脏器组织 ,采用光镜、电镜及脱氧核苷酸末端转移酶介导的缺口末端标记法观察细胞凋亡。结果　内毒素血症时脾、肺、肝、小肠均出现不同程度的实质细胞和免疫细胞细胞凋亡增加 ,而内毒素预处理使上述器官的细胞凋亡明显减少 (P <0 .0 5 )。结论　内毒素预处理可减少大鼠内毒素血症时脾、肺、肝、小肠等脏器的实质细胞及免疫细胞的细胞凋亡 ,这可能是内毒素预处理保护作用的机制之一。     

内毒素预处理对内毒素血症大鼠肺的作用及机制探讨

目的 观察内毒素预处理对内毒素血症大鼠肺的作用及其机制。方法 将雄性Wistar大鼠84只随机分为7组：生理盐水(NS)组,内毒素脂多糖(LPS)2h、4h、6h组和LPS预处理2h、4h、6h组,每组12只。LPS预处理各组大鼠经腹腔注射LPS0．25mg／kg,24h后再注射LPS0．5mg/kg,NS组和LPS各组在上述时间均给予等容量NS;第2次腹腔注射72h后,LPS各组和LPS预处理各组大鼠经静脉注入(静注)LPS 10mg／kg,NS组注射等量NS。NS组在静注NS后6h,LPS2h、4h、6h组和LPS预处理2h、4h、6h组在静注LPS后2、4、6h时各取6只大鼠取血,行血气分析;取左侧肺组织检测细胞间黏附分子-1(ICAM-1)mRNA及抑制性κB-α(IκB-α)蛋白表达;计数右肺支气管肺泡灌洗液(BALF)中白细胞数,测蛋白含量。上述7组另取6只大鼠,在上述相同时点取全肺,计算肺体指数,测定髓过氧化酶(MPO)。结果 LPS各组大鼠较NS组大鼠肺体指数、BALF中白细胞数和蛋白及肺组织MPO含量均增加,氧分压和HCO3^-下降;而LPS预处理各组大鼠上述各指标变化明显减轻。肺组织ICAM-1 mRNA在LPS2h、4h和6h组表达递增,而在LPS预处理各组表达显著减少;LPS2h组肺组织IκB-α蛋白表达较NS组减少,而LPS预处理2h组较LPS2h组表达增加。结论 内毒素预处理可防止内毒素血症时的肺损伤,可能与内毒素预处理使肺组织IκB-α蛋白生成增加和(或)消耗减少有关。     

中度低温对内毒素诱导急性肺损伤大鼠肺泡毛细血管膜通透性的影响

目的探讨中度低温对脂多糖(LPS)诱导急性肺损伤(ALI)大鼠肺泡毛细血管膜通透性的影响。方法34只雄性SD大鼠,随机分为4组。腹腔注射LPS 1.0 mg·kg-1,16 h后在机械通气下气管内滴注1.5 mg·kg-1LPS(0.5 ml)方法建立ALI模型。正常对照组(C组,n=8):只给予等量的生理盐水;内毒素组(L组,n=10):给予LPS;低温组(H组,n=8):将体温降低并维持在32.5-33.0℃, 但不给予LPS;内毒素复合低温组(L H组,n=8):给予LPS,并且当氧合指数(PaO2/FiO2)≤300mm Hg 时将体温降低并维持在32.5-33.0℃。分别于ALI时、ALI后1、2、3、4 h记录平均动脉压(MAP)和中心静脉压(CVP),同时测定动脉血气的变化。于ALI后4 h处死大鼠,检测支气管肺泡灌洗液(BALF) 中白蛋白浓度、左肺湿/干重(W/D)及肺组织髓过氧化物酶(MPO)活性,电镜下观察肺泡毛细血管膜形态结构的变化。结果L组PaO2/FiO2降低(P<0.01),PaCO2在ALI后3、4 h升高(P<0.01);与L组比较,L H组PaO2,FiO2差异无统计学意义,但PaCO2在ALI后3、4 h降低(P<0.05)。与C组比较,L 组BALF中白蛋白浓度、W/D及肺组织MPO活性升高(P<0.01或0.05);而L H组上述指标则较L 组下降(P<0.01或0.05)。电镜结果:C、H组肺泡毛细血管膜结构基本正常;L组毛细血管内皮明显剥脱;而L H组毛细血管内皮剥脱程度较L组减轻。结论中度低温对ALI大鼠可通过减轻肺内PMN聚集,降低肺泡毛细血管膜通透性,在一定程度上减轻了肺损伤。     

盐酸氨溴索预先给药对内毒素诱导大鼠急性肺损伤的作用

目的探讨盐酸氨溴索（AMB）预先给药对内毒素（LPS）诱导大鼠急性肺损伤（ALI）的作用及其机制。方法雄性SD大鼠108只，体重196～273g，12～14周龄。随机分为6组（n=18），A组生理盐水（NS）0．5ml腹腔注射（i．p．）1h后，再i．p．NS0．5ml；B组i．p．AMB 10mg／kg 1h后i．p．NS0．5ml；C组i.p．NS0．5ml 1h后i．p．LPS 5mg／kg；D、E、F组分别i．p．AMB5、10、20mg／kg后1hi．p．LPS5mg／kg。i．p．NS（A、B组）或LPS（C、D、E、F组）后1、2、4h各处死5只大鼠，采用双夹心抗体酶联吸附免疫法测定支气管肺泡灌洗液（BALF）中肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和巨噬细胞炎性蛋白-2（MIP-2）浓度，蛋白印迹法检测肺组织细胞胞浆中磷酸化／非磷酸化c—Jun氨基末端激酶（JNK）的表达。另外3只i．p．NS（A、B组）或LPS（C、D、E、F组）后4h观察大鼠肺组织形态学变化。结果与A组比较，C、D、E、F组BALF中TNF-α、IL-1β和MIP-2升高；与C组比较，E、F组上述三指标均降低。与A组比较，C、D、E、F组磷酸化JNK表达增多；与C组比较，E、F组磷酸化JNK表达减少，D、E、F组非磷酸化JNK表达增多（P〈0．05或0．01）。AMP预先给药可减轻i．p.LPS诱导的肺组织损伤。结论AMB预先给药可减轻LPS诱导大鼠ALI，其机制与抑制肺组织JNK的活化、下调TNF-α、IL-1β和MIP-2的表达有关．且呈剂量依赖性。     

氯胺酮对家兔内毒素性急性肺损伤的影响

目的研究氯胺酮对家兔内毒素(ET)性急性肺损伤(ALI)的影响。方法采用两次注射脂多糖(LPS)的方法复制家兔ALI模型。动物随机分为四组,每组6只:氯胺酮1组(K1组)、氯胺酮2组(K2组)、LPS组(阳性对照)、生理盐水(NS)组(阴性对照),第2次LPS注射后8 h结束实验,测定以下指标变化:支气管肺泡灌洗液(BALF)中白细胞和肺泡上皮细胞计数、肺水含量、肺通透指数(LPI)、肺组织髓过氧化物酶(MPO)含量、肺组织病理。结果LPS组BALF中白细胞和肺泡上皮细胞数量、肺水含量、LPI和肺MPO含量均较NS组明显上升(P<0.01)。NS组肺病理检查正常;LPS组双肺明显肿胀,表面有点片状出血,轻挤切面有水肿液溢出,镜下有明显肺不张和肺泡萎陷,肺间质增厚,内有大量白细胞浸润,肺血管淤血;K1组与K2组前述各指标和病理变化的程度轻于LPS组,其中K2组又明显好于K1组。结论氯胺酮可减轻LPS注射后家兔ALI程度。     

PIAS调控PPARγ的SUMO化修饰在小鼠内毒素性急性肺损伤内源性保护机制中的作用

目的评价小泛素相关修饰物(SUMO) E3连接酶(PIAS)调控过氧化物酶体增殖物激活受体γ(PPARγ)的SUMO化修饰在小鼠内毒素性急性肺损伤(ALI)内源性保护机制中的作用。方法实验Ⅰ清洁级野生型雄性C57BL/6小鼠24只, 6～8周龄, 体质量18～22 g, 采用随机数字表法分为4组(n=6):对照组(C组)、ALI组、ALI+ PPARγ诱导剂TZD组(ALI+T组)、ALI+TZD+SUMO化抑制剂漆树酸组(ALI+T+A组)。尾静脉注射LPS 15 mg/kg制备内毒素性ALI模型。ALI+T+A组注射LPS前1 h时腹腔注射漆树酸5 mg/kg;ALI+T组和ALI+T+A组注射LPS前30 min时腹腔注射TZD 50 mg/kg。给予LPS 12 h后处死小鼠取肺组织, 测定湿重/干重(W/D)比值, 光镜下观察病理学结果, 并行肺损伤评分;分别采用Western blot法和PCR法测定PIAS1、PIAS2、PIAS3和PIASy及其mRNA的表达。实验Ⅱ 体外培养的小鼠肺泡巨噬细胞(MH-S细胞)采用随机数字表法分为4组(n=5):对照组(C组)、LPS...     

异丙酚早期给药对内毒素休克大鼠急性肺损伤的保护作用

目的观察不同时点给予异丙酚对脂多糖(LPS)致内毒素休克大鼠急性肺损伤(ALI)的保护作用及机制.方法静脉注射LPS 8 mg·kg-1复制内毒素致ALI模型,雄性Wistar大鼠76只随机分为5组对照组(A组,n=8)、LPS组(B组,n=17)、异丙酚给药组(C～E组,n=17),C组、D组和E组分别于LPS注入前1 h、LPS注入即刻、LPS注入后1 h、静脉注射异丙酚5 mg·kg-1,继以10mg·kg-1·h-1持续泵注.从注入LPS至实验结束,历时5 h.持续监测平均动脉压(MAP),测定支气管肺泡灌洗液(BALF)中蛋白(BALFpro)、一氧化氮(NO)、肿瘤坏死因子(TNF-α)、肺组织湿/干重比、肺通透指数(PPI)、肺组织中硝基酪氨酸(NT)表达、NT的Westem Blot、肺组织中诱生型一氧化氮合酶mRNA表达及大鼠死亡率.结果与基础值比较,B组、C组、D组、E组在注入LPS后3、5 h MAP降低(P＜0.05),与B组比较,C组、D组注入LPS后5 h MAP降低(P＜0.05).与A组比较,B组、D组、E组PPI、W/D、BALFpro及BALF中TNF-α、NO均升高(P＜0.01),C组W/D、BALFpro及BALF中TNF-α、NO升高(P＜0.01);与B组比较,C组、D组PPI、W/D、BALFpro及BALF中TNF-α、NO均降低(P＜0.05或0.01),E组W/D、BALFpro及BALF中NO降低(P＜0.05).与B组比较,A组NT微弱表达,B组表达明显增强,C组、D组、E组表达减弱,以C组最明显.与B组比较,C组、D组、E组吸光度比值降低(P＜0.01).A组、B组、C组、D组、E组大鼠死亡率分别为0%、64.7%、11.8%、23.5%和41.2%.结论异丙酚早期给药对内毒素致ALI有保护作用.     

p38MAPK信号转导通路在大鼠内毒素性急性肺损伤中的作用

目的 探讨p38丝裂原活化蛋白激酶(p38MAPK)信号转导通路在大鼠内毒素性急性肺损伤中的作用.方法 成年雄性SD大鼠60只,体重180～230 g,采用随机数字表法,将大鼠随机分为4组:对照组(C组,n=6)、急性肺损伤组(ALI组,n=24)、p38MAPK特异性抑制剂SB203580+ALI组(SB+ALI组,n=24)和SB203580组(SB组,n=6).ALI组尾静脉注射内毒素5 mg/kg制备大鼠急性肺损伤模型,C组给予等容量生理盐水,SB+ALI组于注射内毒素前30 min经尾静脉注射SB20358010 mg/kg.ALI组和SB+ALI组于注射内毒素后1、3、6 h(T1-3)时随机取8只大鼠,C组和SB组分别于给予生理盐水、SB203580后1 h处死取肺组织,检测磷酸化p38MAPK(p-p38MAPK)蛋白表达.T3时回收支气管肺泡灌洗液(BALF),测定蛋白浓度.计算细胞凋亡指数,观察肺组织病理学结果.另取32只大鼠,采用随机数字表法,将大鼠随机分为2组(n=16):ALI组和SB+ALI组,观察48 h内大鼠生存情况.结果 与C组相比,ALI组和SB+ALI组BALF中蛋白浓度、细胞凋亡指数、肺组织p-p38MAPK蛋白表达水平升高(P＜0.05);与ALI组相比,SB+ALI组上述指标降低(P＜0.05).SB+ALI组病理学损伤程度较ALI组明显减轻.ALI组大鼠生存率较SB+ALI组降低(P＜0.01).结论 p38MAPK信号转导通路参与了大鼠内毒素性急性肺损伤的发生和发展,可能与肺组织细胞凋亡有关.

Abstract：

Objective To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods Sixty male SD rats weighing 180-230 g were randomly divided into 4 groups: control group (group C, n = 6), ALI group ( n = 24),p38MAPK specific inhibitor SB203580 + ALI group (group SB + ALI, n = 24), SB203580 group (group SB,n =6). LPS 5 mg/kg was injected intravenously via tail vein in group ALI and SB + ALI, while the equal volume of normal saline was given instead in group C. Group SB + ALI received iv injection of SB203580 10 mg/kg via tail vein 30 min before LPS administration. Group SB received injection of SB203580. The rats were sacrificed at 1, 3 and6 h agter LPS administration (T1-3) in group ALI and SB + ALI (8 rats at each time point) andat 1 h after administration in C and SB groups. The lungs were immediately removed for microscopic examination and determination of phosphorylated p38MAPK (p-p38MAPK) expression, the concentration of protein in bronchoalveolar lavage fluid (BALF) and apoptotic index (AI). Another 32 rats were selected and randomly divided into 2 groups for survival study: ALI group and SB + ALI group ( n = 16 each), and then they were treated as mentioned above and observed for 48 h. Results The concentration of protein in BALF, AI and p-p38MAPK expression were significantly increased in group ALI and SB + ALI compared with group C, while decreased in group SB + ALI compared with group ALI ( P ＜ 0. 05 ). LPS-induced pulmonary histological changes were significantly attenuated in group SB + ALI compared with group ALI. The survival rate was significantly decreased in group ALI compgred with group SB + ALI ( P ＜ 0.01 ). Conclusion p38 MAPK signal transduction pathway is involved in LPS-induced ALI, which may be related to the apoptosis in the cells in the lung.     

内毒素预处理对内毒素血症大鼠心脏的作用及机制

目的 观察内毒素预处理对内毒素血症大鼠心脏的作用并探讨其机制。方法 雄性Wistar大鼠60只,随机分为三组:生理盐水组(N组,n=12);LPS对照组(L组,n=24)和LPS预处理组(P组,n=24),P组:首次,经腹腔注射LPS 0.25mg/kg,24h后再经腹腔注射LPS 0.5mg/kg,其余两组在上述时间均给予等量生理盐水(NS);在第一次腹腔注射96h后,L组和P组静脉注入LPS10mg/kg,N组给予等量NS,每组各取6只大鼠用于连续观察心肌收缩力各指标。另外,N组取6只在6h末取血处死大鼠,L组和P组分别在静注2、4、6 h时各取6只大鼠取血处死动物。用于测定心脏生化指标及免疫组化染色检测HSP70蛋白表达。结果 L组大鼠的心肌收缩力指标LVSP和±dp/dt max在静注LPS1h后较N组明显降低(P<0.05),而P组较L组增加,与N组相比无显著统计学意义。L组血浆中LDH浓度、CK活性随时间延长较N组逐渐增加,而P组上述指标较L组明显降低(P<0.05),与N组相比无明显差异。L组大鼠HSP70蛋白表达较N组有增加趋势,但与N组相比无显著统计学意义;而P组HSP70蛋白表达在2、4、6 h较N组增加,在6 h较L组显著增加。结论 内毒素预处理可防止内毒素对心脏的损伤作用,可能与诱导心脏HSP70的表达,增强组织抗损伤能力有关。     

异丙酚对内毒素所致急性肺损伤大鼠肺组织TGF-β1/Smad2信号通路的影响

目的 探讨异丙酚对内毒素所致急性肺损伤大鼠肺组织转化生长因子(TGF)-β1/Smad2信号通路的影响.方法 健康雄性Wistar大鼠56只,7～8周龄,260 ～ 300 g,采用随机数字表法,将其随机分为5组:正常对照组(A组,n=8)、LPS组(B组,n=12)、异丙酚不同时点给药组(C组～E组,n=12).A组给予等容量生理盐水,B组静脉注射脂多糖8 mg/kg,C组、D组和E组分别于给予LPS前1h、给予LPS后即刻和给予LPS后1h时静脉注射异丙酚5 mg/kg,随后以10 mg· kg-1·h-1速率输注至给予LPS后5h.分别于给予LPS前即刻、给予LPS后1、3、5h时采集动脉血样,测定pH值和PaO2,随后处死大鼠,取肺组织,计算湿/干重比(W/D),测定肺组织TGF-β1 mRNA和Smad2表达.结果 与A组比较,B组和E组pH值和PaO2降低,肺组织W/D升高,TGF-β1 mRNA和Smad2表达上调(P＜0.05);与B组比较,C组和D组pH值和PaO2升高,肺组织W/D降低,TGF-β1 mRNA和Smad2表达下调,E组PaO2升高(P＜0.05).结论 异丙酚减轻内毒素所致ALI的机制与抑制TGF-β1/Smad2通路激活有关.     

2015年乳腺癌辅助化疗进展

【摘要】〓乳腺癌是危害我国女性健康的头号杀手,尽管近年来辅助化疗的研究进展突飞猛进,但临床中仍有不少问题未能明确,如辅助化疗的合适人群、化疗的开始时间、蒽环及紫杉类的地位和用法、强化维持治疗的作用、疗效及预后的生物标志物等。本文结合乳腺癌辅助化疗在临床上的常见问题和2015年各大乳腺癌会议阐述乳腺癌辅助化疗的最新进展。     

Alterations in T-Cell Subset Frequency in Peripheral Blood in Obesity

Background: Obesity affects the regulation of immune and inflammatory responses. This study characterizes differences in peripheral blood lymphocyte phenotype in obese humans. Methods: Frequencies of lymphocyte subsets among peripheral blood mononuclear cells were compared between 10 obese (BMI ≥35) and 10 lean subjects, as determined by antibodies directed against cluster differentiation (CD) markers. Results: Obese patients demonstrated an increased frequency of CD3+CD4+ T-cells (mean difference 12%, P=0.004), a decreased frequency of CD3+CD8+ T-cells (mean difference 9.4%, P=0.016) and an increased frequency of CD3+CD8+CD95+ T-cells (mean difference 13.3%, P=0.032). No other differences among T-cell or monocyte subsets were noted. Conclusions: Obesity is associated with alterations in frequencies of peripheral CD4+ and CD8+ T-cells and aberrations in the expression of CD95 among CD8+ T-cells. These data suggest both CD4+ and CD8+ T-cell compartments, as well as the regulation of CD95 expression on CD8+ T-cells, as targets for further study into obesity's effects on the immune system.     

西宁地区烧伤病人动脉血气分析观察

对高海拔地区的27例烧伤病人动脉血气变化进行了分析和观察。结果证明:无论是存活病人还是死亡病人伤后均存在有低氧血症问题。并且在死亡病人和烧伤合并吸入性损伤病人其低氧血症的发生早于单纯烧伤病人。提示:吸入性损伤病人应立即行气管切开术以保障氧气供给,单纯烧伤病人可常规吸氧以维持正常血 PaO_2,ARDS 均发生在合并吸入性损伤的病人,高频喷射通气技术对纠正低氧血症有一定效果。     

Controversies in Fistula in Ano

Managing a complex fistula in ano can be a daunting task for most surgeons; largely due to the two major dreaded complications—recurrence & fecal incontinence. It is important to understand the anatomy of the anal sphincters & the aetiopathological process of the disease to provide better patient care. There are quite a few controversies associated with fistula in ano & its management, which compound the difficulty in treating fistula in ano. This article attempts to clear some of those major controversies.     

β-半乳糖苷酶在体内外成骨细胞中的表达

目的 研究β—半乳糖苷酶(β—gal)在成骨细胞中的表达状况，为阐明MorquioB综合征的发病机制提供依据。方法 裸鼠各器官和骨组织标本行X-gal染色检测。抽取羊和人骨髓行骨髓基质细胞(BMSCs)培养，分为4组：I：Adv-hBMP-2转染组；Ⅱ：Adv—β—gal转染组；Ⅲ：未转染组；Ⅳ：地塞米松诱导组。分别行X-gal染色和RT-PCR检测β—gal的表达。结果 裸鼠骺板两侧、骨膜内面及松质骨的成骨细胞和破骨细胞可见多量β—gal的表达。未转染BMSCs组有少量β—gal的表达，其他3组细胞的β—gal表达增高。结论成骨细胞和破骨细胞可表达多量β—gal，该两种细胞的β—gal缺乏可能是MorquioB综合征骨骼异常的直接原因。     

Smoking-Attributable mortality in Spain in 2016

IntroductionSmoking-attributable mortality (SAM) is a valuable indicator that can be used to characterize the course and health burden of the smoking epidemic. The aim of this paper was to estimate SAM in Spain in 2016 in the population aged 35 and over, using the best available evidence.MethodsA smoking prevalence-dependent analysis based on the estimation of population-attributable fractions was performed. Smoking prevalence (never, former, and current smokers) was calculated from a combination of the Spanish Health Survey (2016) and the European Health Survey (2014); the relative risk of death among current and former smokers was taken from the follow-up of various cohorts; and mortality rates were obtained from National Center for Statistics data. SAM estimates are presented globally, and by sex, age groups, and major disease categories: cancer, cardiometabolic diseases and respiratory diseases.ResultsIn 2016, 56,124 deaths were attributed to tobacco consumption, 84% in men (47,000), and 50% in the population aged over 74 (27,795). Overall, 50% of SAM was due to cancer (28,281), 65% of which was lung cancer. One in 4 attributable deaths (13,849) occurred before the age of 65.ConclusionsOne in 7 deaths in Spain in 2016 were attributable to smoking. This estimation of SAM clearly highlights the great impact of smoking on mortality in Spain, mainly due to lung cancer and chronic obstructive pulmonary disease.     

MicroRNAs in hepatic pathophysiology in diabetes

MicroRNAs(miRNAs or miRs) are small approximately 22 nucleotide RNA species that are believed to regulate diverse metabolic and physiological processes.In the recent past,several reports have surfaced that demonstrate the role of miRNAs in various biological processes and numerous disease states.For a disease as complex as diabetes,the emergence of miRNAs as key regulators leading to the disease phenotype has added a novel dimension to the area of diabetes research.On the other hand,the liver,a metabolic hub,contributes in a major way towards maintaining normal glucose levels in the body as it can both stimulate and inhibit hepatic glucose output.This equilibrium is frequently disturbed in diabetes and hence,the liver assumes special significance considering the correlation between altered hepatic physiology and diabetes.While the understanding of the mechanisms behind this altered hepatic behavior is not yet completely understood,recent reports on the status and role of miRNAs in the diabetic liver have further added to the complexities of the knowledge of hepatic pathophysiology in diabetes.Here,we bring together the various miRNAs that play a role in the altered hepatic behavior during diabetes.     

Fluid-phase transcytosis in the primate epididymis in vitro and in vivo

Ligated tubules from the corpus epididymidis of men and monkeys were incubated in medium containing horseradish peroxidase (HRP) as a marker for fluid-phase endocytosis. HRP was localized by light and electron microscopy after 0, 15, 30 and 60 min of incubation. Movement between the cells was prevented by tight junctions, but bypass of this barrier was apparently achieved by an intracellular vesicular mechanism leading to a time-dependent appearance of HRP in the lumen. Uptake of HRP into basal cells and capture by the lysosomal apparatus of principal cells were also observed. HRP-filled vesicles also appeared in the basal, mid and apical cytoplasm of epithelial cells in the caput 1 h after injection of the tracer into the epididymal circulation of the monkey, suggesting that this pathway also operates in vivo.