含血栓的曲张大隐静脉管壁滋养血管分布与定量研究

目的 探讨含血栓的曲张大隐静脉血管壁滋养血管增生情况.方法 收集含血栓的曲张大隐静脉管壁标本11份（血栓组）,单纯曲张大隐静脉管壁标本11份（曲张组）,另设正常大隐静脉管壁标本8份作为对照（对照组）.Masson染色观察3组血管壁中滋养血管的分布与密度.结果 血栓组血管壁外膜滋养血管明显增多,呈簇状聚集;中膜呈线性增多;内膜见散在的滋养血管,部分被血栓破坏断裂的内膜中滋养血管呈增多现象.与曲张组、对照组比较,血栓组静脉管壁全层滋养血管数量增加,组间比较差异有统计学意义（P 〈 0.05）;各组内外膜与中膜、内膜比较差异亦有统计学意义（P 〈 0.05）,中膜与内膜比较差异无统计学意义.结论 静脉高压和缺氧是导致静脉血栓形成的启动因素,静脉血栓形成可能会加重血管壁滋养血管的重塑.     

含血栓的曲张静脉血管壁T和B淋巴细胞浸润的定量研究

目的：探讨含血栓的曲张大隐静脉血管壁T、B淋巴细胞的浸润情况。方法：收集单纯曲张大隐静脉管壁标本11例,含血栓的曲张大隐静脉管壁标本11例,另设8例正常大隐静脉管壁标本作对照,行免疫组织化学染色,观察血管壁中T、B淋巴细胞的分布。结果：血栓组管壁各层中T、B淋巴细胞呈现＂聚集性＂增多;曲张组在滋养血管周围可见少量淋巴细胞浸润。血栓组T、B淋巴细胞计数与曲张组、对照组差异均有统计学意义（P〈0.01）,曲张组与对照组之间差异无统计学意义（P〉0.05）。结论：静脉血栓形成可诱发静脉血管壁T、B淋巴细胞的重塑。     

含血栓静脉管壁病理形态学特征的比较性研究

目的 探讨含血栓的静脉管壁病理形态学特征及管腔内径变化.方法 收集含血栓的曲张大隐静脉主干标本18例(血栓组),单纯曲张大隐静脉主干标本18例(曲张组),另设正常大隐静脉主干标本12例(对照组).采用苏木精-伊红和Masson染色法,观察管壁组织结构,测量血管壁内径与内膜、中膜、外膜厚度.结果 血栓组管壁全层及血栓内见大量炎细胞浸润,血栓附着处内皮细胞缺失,大量增生的胶原纤维自破裂内膜处延伸至血栓内致部分血栓机化.曲张组管壁全层偶见炎细胞,内膜增厚,中膜平滑肌细胞不规则增生,排列紊乱,胶原纤维增生.对照组管壁内膜薄,中膜平滑肌束排列规则.血栓组管腔内径、内膜厚度、中膜厚度和外膜厚度与曲张组、对照组比较差异均有统计学意义(P＜0.05),曲张组管腔内径和内膜厚度与对照组比较差异有统计学意义(P＜0.05).结论 含血栓的曲张静脉管腔增大、管壁增厚是病理形态学改变的主要特征.     

大隐静脉曲张管壁肥大细胞浸润分布与定量研究

目的探讨在不同病期、不同部位血管壁中肥大细胞浸润与大隐静脉曲张(VGSV)的关系。方法收集19例曲张大隐静脉的主干上、中、下3段管壁标本,其中曲张静脉伴有皮肤营养改变9例,单纯曲张静脉10例,另设9例正常静脉作对照,行甲苯胺蓝特殊染色。观察管壁中的肥大细胞浸润分布与计数情况。结果研究组肥大细胞的分布,内膜或中膜均可见少数肥大细胞,外膜则较多聚集。上、中、下3段血管壁肥大细胞计数结果:皮肤改变组(0.26±0.08)/HP、(0.24±0.18)/HP、(0.30±0.05)/HP;曲张组(0.26±0.12)/HP、(0.15±0.03)/HP、(0.12±0.05)/HP;对照组(0.23±0.14)/HP、(0.36±0.30)/HP、(0.27±0.16)/HP。各组间、段间的肥大细胞计数差异均无统计学意义。结论在不同病期、不同部位血管壁中肥大细胞的浸润㈦大隐静脉曲张的程度不存在量的变化关系。     

含血栓曲张大隐静脉管壁中膜胶原和弹性纤维的分布与定量研究

目的:探讨含血栓曲张大隐静脉血管壁中膜胶原纤维和弹性纤维的变化。方法:收集含血栓曲张大隐静脉管壁标本19例(血栓组),单纯曲张大隐静脉管壁标本10例(曲张组),另设17例正常大隐静脉管壁标本作对照(对照组)。行EVG染色,光学显微镜下进行管壁中膜胶原和弹性纤维分布观察和图像定量分析。结果:血栓组胶原纤维明显增多、堆积,部分增生的胶原纤维侵入并破坏平滑肌细胞规则性环层排列,弹性纤维明显减少,环形分布被破坏,出现分离、断裂。血栓组胶原纤维的相对含量(RCC)、弹性纤维的相对含量(RCE)以及管壁僵硬度(C/E)分别为(41.90±10.91)%、(2.44±1.54)%和25.22±18.97;曲张组为(29.71±6.63)%、(7.50±2.49)%和4.34±1.42;对照组为(23.52±6.20)%、(9.71±3.89)%和2.59±0.83。血栓组RCC、RCE、C/E与曲张组和对照组比较差异均有统计学意义(P<0.01)。结论:静脉血栓形成可能会加重管壁中膜胶原和弹性纤维的比例失调。     

曲张大隐静脉管壁滋养血管分布与定量研究

目的探讨在不同病期、不同部位血管壁中滋养血管变化与大隐静脉曲张(GSVV)病期的关系。方法 19例GSVV患者,其中曲张静脉伴皮肤营养改变9例(皮肤改变组),单纯曲张静脉10例(曲张组)。分别取其曲张大隐静脉主干上、中、下三段管壁标本,另设9例正常静脉作对照(对照组);行苏木素-伊红染色,观察管壁中的滋养血管分布和密度情况。结果皮肤改变组、曲张组外膜和中膜外层见滋养血管明显增多。滋养血管密度测定:皮肤改变组、曲张组管壁中滋养血管密度明显高于对照组,差异有统计学意义(P<0.05);三组内上、中、下三段各段间滋养血管密度差异均无统计学意义(P>0.05)。结论曲张大隐静脉主干管壁中滋养血管分布和密度与病期和部位不存在量的变化关系。曲张静脉管壁外膜和中膜滋养血管增多,推断可能与静脉高压、缺氧导致血管壁重塑有关。     

高血流动力对大隐静脉和脾静脉血管重塑的影响

目的探讨高血流动力对大隐静脉和脾静脉血管重塑的影响.方法收集曲张大隐静脉和门静脉高压性脾静脉管壁标本34例,设正常大隐静脉和脾静脉14例为对照组,光学显微镜下观察HE染色和Masson染色后的大隐静脉、脾静脉管壁组织学改变.结果 HE染色曲张大隐静脉管壁呈不均匀性增厚改变,高压性脾静脉呈均匀性增厚改变;Masson染色管壁增厚,以内膜、中膜肌层和纤维结缔组织增生为主,曲张的大隐静脉（2/20）内膜轻度黏液样变性,高压性脾静脉（5/14）重度黏液性变性.结论高血流动力学影响大隐静脉和脾静脉管壁的重塑,提示内脏静脉比外周静脉病理改变更明显.     

曲张大隐静脉管壁细胞凋亡水平的变化

目的:观察不同部位曲张大隐静脉管壁细胞的凋亡水平的变化.方法:收集21例曲张大隐静脉(观察组)与12例正常大隐静脉(对照组),分别采用TUNEL法和免疫荧光法检测各自上、中、下3段管壁的细胞凋亡情况.结果:观察组管壁(内膜和中膜)偶见单个凋亡细胞,且3段分布基本相同,对照组管壁(内膜和中膜)各段则见较多凋亡细胞,且上段较下段更为明显.定量分析显示,观察组各段的内膜或中膜的细胞凋亡率均明显低于对照组的相应区域(均P＜0.05);两组组内各段间细胞凋亡率比较,部分有统计学差异(P＜0.01或P＜0.05),总体趋势,上段高于下段,内膜高于中膜.结论:曲张大隐静脉管壁细胞凋亡明显下调,且无正常大隐静脉管壁凋亡水平的节段间差异.     

高流体静力压下大隐静脉和脾静脉管壁滋养血管对比研究

目的：观察高流体静力压对大隐静脉和脾静脉管壁滋养血管的影响。 方法：收集曲张大隐静脉和高压性脾静脉标本（疾病组）,以及正常大隐静脉和脾静脉标本（正常对照组）。采用CD34免疫组化染色与Masson染色,计算各组管壁滋养血管的数量和平均截面积,并定量分析。 结果：形态学观察显示,两个疾病组管壁滋养血管均较各自的对照组明显增生。定量分析显示,两个疾病组的滋养血管数量、平均截面积在中膜或外膜,均明显大于各自的正常对照组（均P<0.05）;脾静脉外膜滋养血管数量疾病组与其正常对照组差值明显大于大隐静脉,大隐静脉外膜滋养血管疾病组与其正常对照组平均截面积差值明显大于脾静脉（均P<0.05）,但两种血管间以上差值在中膜中的差异均无统计学意义（均P>0.05）。 结论：高流体静力压下大隐静脉和脾静脉管壁滋养血管明显增生,两者变化存在异质性,大隐静脉中以管径增大为主,脾静脉中以数量增多为主。     

曲张大隐静脉管壁病理形态学特征研究

目的检测曲张大隐静脉管壁各参数,并探讨曲张大隐静脉管壁发生、发展过程中组织形态学特征与临床病期之间的关系。方法回顾性分析我院2008年7月至2009年7月期间收治的49例高位结扎剥脱加旋切治疗的大隐静脉曲张患者的临床资料,按临床CEAP分级分为单纯静脉曲张组(C2~C3级,简称单纯曲张组),24例;静脉曲张并皮肤改变组(C4~C6级,简称皮肤改变组),25例;另选6例因外伤行截肢术但大隐静脉正常无损伤者作为对照组。采用Masson染色测量静脉内膜和中膜厚度,以测量静脉截面的最大直径作为管腔内径值,采用免疫组织化学SP法观察静脉管壁的结构变化。结果管腔内径:与对照组比较,单纯曲张组及皮肤改变组上、中、下三段静脉管腔内径均明显增大(P<0.05);皮肤改变组上、中段静脉管腔内径较下段也明显增大(P<0.05);单纯曲张组三段静脉管腔内径变化差异无统计学意义(P>0.05)。单纯曲张组和皮肤改变组的静脉管壁结构改变大致相似,主要表现为内膜不均匀增厚,管壁厚薄不等,以胶原纤维和细胞外基质增生为主,伴有平滑肌增生,中膜厚度略增加,平滑肌束排列紊乱,部分萎缩、凋亡,部分局灶增生,肌束间纤维胶原间质增生,两者相互穿插,排列混乱,弹力纤维断裂。皮肤改变组还可见内膜继发性改变,包括黏液变性、玻璃样变性、内膜炎、血栓形成等。单纯曲张组和皮肤改变组上、中、下三段静脉内膜厚度明显大于对照组(P<0.05);单纯曲张组上、下段静脉内膜厚度明显小于中段(P<0.05);单纯曲张组中段内膜厚度明显大于皮肤改变组中段(P<0.05)。中膜厚度单纯曲张组、皮肤改变组和对照组之间以及同一组内上、中、下三段间比较差异均无统计学意义(P>0.05)。结论下肢曲张静脉管腔扩张,内膜增厚,内膜改变以中段出现较早且显著,上、下二段血管壁的重塑与临床病期之间无关。     

Dysregulated apoptosis in primary varicose veins.

OBJECTIVE: Programmed cell death plays a critical role in various physiological processes. To investigate its possible pathogenic role in primary varicose veins we studied histological changes in surgical specimens from human varicose veins. In varicose and healthy veins, we also determined the number of cells in apoptosis, and investigated mediators regulating the intrinsic apoptotic mitochondrial pathway (Bax and caspase 9). METHODS: A total 23 varicose veins were obtained from 18 patients undergoing lower-extremity varicose vein surgery for primary varicose disorders. We used nine healthy veins obtained from nine patients undergoing distal arterial bypass grafting surgery as controls. The venous segment analysed was the distal part of the greater saphenous vein. Specimens for histological examination were stained with hematoxylin and eosin, trichromic and Victoria blue. Cell apoptoses and mediators of the mitochondrial pathway were detected in the media by immunohistochemistry using antibodies to peroxidase in situ apoptosis, Bax and caspase 9. Results were expressed as indexes for the three antibodies tested. The Mann-Whitney test was used to compare the results obtained in the two groups. RESULTS: Varicose vein specimens exhibited a more disorganised architecture than healthy veins and showed an increased number of collagen fibres and a decrease in the density and size of elastic fibres. All anti-apoptotic antibodies tested detected significantly fewer immunoreactive cells in tissue sections from the media of varicose veins than of healthy veins (peroxidase in situ, varicose veins (VV) median 2.4% (inter-quartile range 1.6-3.9) versus control (C) 14% (IQR 8.8-19); Bax, VV 1.4% (IQR 0.36-2.4) versus C 11% (IQR 7.6-15); and caspase 9, VV 1.7% (IQR 0.06-3.4) versus C 10% (IQR 9.1-12), P=0.0001 (Mann-Whitney test). CONCLUSION: Apoptosis is down regulated in the medial layer of varicose veins. This dysregulation of the cellular mechanism that maintains normal tissue integrity is mediated through the intrinsic apoptotic pathway and may be among the causes of primary varicose veins.     

Expression of molecular mediators of apoptosis and their role in the pathogenesis of lower-extremity varicose veins

PURPOSE: In an earlier study, we observed a significant decrease in apoptosis in varicose veins, as compared with healthy veins, indicating that deregulated apoptosis plays a role in the pathogenesis of varicosities. In addition, significant differences were noted in the expression and subcellular localization of the cell cycle regulatory protein, cyclin D1 in varix tissues, as compared with controls. Because cell cycle checkpoint controls are linked to the signaling and execution of apoptotic cascades, we examined the expression of bcl-2 family members bax and bcl-x, known molecular mediators of apoptosis, and that of poly (ADP-ribose) polymerase (PARP), a downstream substrate of DNA cleavage. METHODS: Twenty varicose vein specimens were retrieved from 20 patients (10 men, 10 women; mean age, 53.6 +/- 4.7 years) undergoing lower-extremity varicose vein excision. Healthy greater saphenous vein segments (n = 27) were obtained from 27 patients (14 men, 13 women; mean age, 59.5 +/- 2.4 years) undergoing infrainguinal arterial bypass grafting surgery. All tissues were distal portions. As per CEAP classification for chronic lower-extremity venous disease, most of the patients were in class 2 for clinical signs (n = 11); some patients were in class 3 (n = 4) or class 4 (n = 4), and only one patient was in class 5. Five 5-microm thick sections from formalin-fixed, paraffin-embedded specimens were used as a means of immunohistochemically localizing the expression of bax, bcl-x, and PARP, and 10 random high-power fields per section were evaluated by two independent reviewers blinded to the clinical findings. Statistical analyses were conducted by means of chi(2), analysis of variance, Student and Fisher exact t tests with StatView software. RESULTS: Immunoreactivity to pro-apoptotic bax was significantly higher in the normal veins (P <.001). Cytoplasmic expression of bcl-x was prominent in the cells of the vasa vasorum in both varicose and healthy veins. PARP expression was diminished in the varicose vein group, with 2.8 +/- 0.7 (P =.01) and 1.4 +/- 0.5 (P =.05) cells per high-power field in the intima and media, respectively. Neither bax nor PARP was noted in the adventitia of varicose veins, although their expression was detected in this layer of the control group (P <.001). CONCLUSION: The entry of smooth muscle cells into the apoptotic pathway may be regulated by the induction of bax in this model, because there is significant presence of this pro-apoptotic protein in healthy veins. Both bax and PARP are downregulated in varicose veins, as compared with healthy veins, and this may play a significant role in the pathogenesis of varicose veins.     

Immunocytochemical characterisation of the inflammatory cell infiltrate of varicose veins.

OBJECTIVES: To characterise the inflammatory cell infiltrate in varicose vein wall, and its relationship to the valve complex. DESIGN: A comparative study of the distribution of inflammatory cells in normal and varicose vein. MATERIALS: Specimens of proximal human long saphenous vein were obtained from patients with duplex Doppler confirmed long saphenous vein reflux (n=14). Control vein was obtained from patients undergoing coronary artery bypass without clinical evidence of venous insufficiency (n=6). Longitudinal 7 microm frozen sections of vein, displaying valve, were prepared. METHODS: Using immunohistochemistry, T-lymphocytes (CD3), macrophage/monocytes (CD68), neutrophils (CD15s) and mast cells (anti-mast cell tryptase) were identified. The number of cells per unit length vein were counted using light microscopy. RESULTS: There were significantly more mast cells and macrophage/monocytes in varicose vein as compared to control. There was a non-significant trend towards more T-lymphocytes in varicose vein. Few neutrophils were present in varicose or normal vein. The distribution of inflammatory cells with respect to the valve was not found to be significant. CONCLUSIONS: Varicose veins display a greater inflammatory cell infiltrate than normal vein. The key role of macrophage/monocytes and mast cells in tissue damage and remodelling should stimulate further research into whether they play a significant role in the development of chronic venous insufficiency.     

消炎膏治疗下肢静脉曲张泡沫硬化剂联合手术治疗后血栓性浅静脉炎的临床效果

目的:探讨消炎膏治疗下肢静脉曲张泡沫硬化剂联合手术治疗后血栓性浅静脉炎的有效性。方法:选取2017年1月—2020年1月于济南市中医医院周围血管病科接受下肢静脉曲张泡沫硬化剂联合手术治疗后出现血栓性浅静脉炎的患者60例,采用随机数字表法随机分为观察组和对照组,每组30例。在常规治疗基础上,观察组应用本院外用自制剂消炎膏外敷治疗,对照组采用多磺酸黏多糖乳膏治疗,比较两组患者治疗前后的症状评分、血栓长度、炎性面积及疼痛评分。结果:两组患者治疗后的皮肤颜色、肿胀程度、皮肤温度及疼痛程度症状评分,血栓长度、炎性面积、患处皮肤温度及疼痛评分较治疗前均有显著降低(P<0.05);观察组患者症状评分、血栓长度、炎性面积及患处皮肤温度小于对照组,差异有统计学意义(P<0.05);两组患者治疗后疼痛评分差异无统计学意义(P>0.05)。结论:消炎膏和多磺酸黏多糖乳膏对下肢静脉曲张泡沫硬化剂联合手术治疗后血栓性浅静脉炎的治疗均有效,但消炎膏在改善临床症状、缩短血栓长度和减小炎性面积方面优于多磺酸黏多糖乳膏。     

新基因nelin在下肢曲张静脉中的表达及其意义

目的：从基因的转录和翻译水平探讨nelin在下肢曲张静脉中的表达及意义。方法：分别利用RT-PCR技术以及免疫组织化学技术比较静脉曲张患者（实验组）以及正常人（对照组）之间大隐静脉血管组织中nelin基因及其蛋白的表达水平。结果：实验组的病变静脉组织中,nelin的表达低于对照组。RT-PCR显示,实验组与对照组目的条带亮度不同,对照组较实验组亮;免疫组织化学显示,对照组中nelin蛋白大量分布于正常静脉管壁血管平滑肌细胞的胞质,呈棕黄色,平均阳性细胞百分比为（80.67±10.20）%;而实验组中染色较弱,呈浅黄色,平均阳性细胞百分比为（18.39±7.78）%,差异有统计学意义（P〈0.01）。结论：与正常人相比,原发性下肢静脉曲张患者的病变静脉组织中nelin基因在转录和翻译水平均存在明显的表达下调,这可能与病变静脉组织的形态学改变有一定的关系。