睾丸鞘膜瓣在尿道修复中的应用

目的探讨睾丸鞘膜瓣覆盖技术在尿道畸形和尿道瘘修复中的效果。方法2002年起对38例尿道下裂手术和术后尿道瘘,采用睾丸鞘膜下组织蒂鞘膜瓣覆盖修复。结果术后随访半年至1年,除1例尿道上裂术后瘘修复后再次发生尿道瘘外,其余均获成功,未再出现尿道瘘或尿道狭窄,阴茎外观满意,勃起正常。结论采用该方法可有效防止尿瘘再发生,提高手术成功率且易于获取,对睾丸无不良影响。     

兔腹主动脉球囊成形术后狭窄过程中内皮素的动态变化及卡托普利的治疗作用

目的　观察内膜损伤后血管狭窄的主要病理变化和此过程中血浆内血管内皮素(endothelin ,ET)水平的动态变化及局部动脉组织内ET反应性 (ET immunoreaction ,ET IR) ,探讨卡托普利 (Captopril)对动脉球囊损伤后狭窄的影响。方法　大耳白兔 4 8只 ,依术后处死时间不同 (6h和 1、3、7、15、2 2d)按随机表法随机分为 6组 ,每组 8只 ,其中 3只为内膜损伤 (手术组 )、3只为损伤 卡托普利治疗 (治疗组 ) ,2只为对照组。术前及术后均采静脉血 ,手术组及治疗组置入微球囊导管于腹主动脉内制备内膜损伤模型。治疗组术前 1d给予卡托普利 2mg·kg-1·d-1直至处死当日。放射免疫法检测术前、术后血浆内ET水平 ,处死后取模型动脉血管 ,观察血管内膜厚度及管腔病理变化 ,免疫组织化学法检测动脉组织内ET反应。结果　手术组各时间段血浆ET水平 [平均值 (139 17± 16 86 )ng/L) ]和治疗组各时间段血浆ET水平 [平均值 (12 2 16± 13 5 6 )ng/L]均较术前 [平均值 (111 2 4±11 39)ng/L]升高 (P <0 0 1和P <0 0 5 ) ,手术组术后各时间段血浆ET水平比治疗组及对照组有明显升高 (P值均 <0 0 1) ,而治疗组与对照组术后血浆ET水平无显著性差异 ;手术组动脉内膜有不同程度增厚 ,主要以血管平滑肌细胞 (vascularsmoothmusclec     

Long term changes in the vascular wall after laser recanalization of an artery

All-Union Surgical Research Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. N. Malinovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 12, pp. 653–657, December, 1991.     

Expression of cell cycle regulators during smooth muscle cell proliferation after balloon catheter injury of rat artery

Intimal hyperplasia is defined as the abnormal migration and proliferation of vascular smooth muscle cells (VSMCs) with deposition of extracellular matrix. However, the cell cycle regulatory mechanisms of injury-induced VSMC proliferation are largely unknown. To examine the expression kinetics of cell cycle regulatory factors which is known to be worked positively or negatively, we used rat balloon injury model. Marked induction of proliferating cell nuclear antigen (PCNA), G1/S cyclin-dependent kinase (cdk2), and its regulatory subunit (cyclin E) occurred between 1 and 3 days after balloon arterial injury, and this was sustained for up to 7 days and then declined. However, the induction of the negative regulators, p21 and p27, occurred between 3 and 5 days of injury, peaked after 7 and 14 days and was then sustained. VSMC proliferation after balloon catheter injury of the rat iliac artery is associated with coordinated expression of positive (cdk2, cyclin E and PCNA) and negative (p21, p27) regulators. Cell cycle regulators such as cdk2, cyclin E, p21, p27 may be suitable targets for the control of intimal hyperplasia.     

菲律宾蛤仔饮食对兔实验性动脉粥样硬化形成的影响

目的评价菲律宾蛤仔饮食对兔实验性动脉粥样硬化形成的影响。方法在普通低脂饮食和高脂饮食基础上加用菲律宾蛤仔饮食 ,喂养动物 8周 ,观察菲律宾蛤仔饮食对于动物血脂、主动脉粥样硬化斑块面积比和主动脉根部内膜中膜厚度比值 (IMT)的影响。结果 8周末 ,与对照组相比 ,正常饲料中加入RP的动物组血脂浓度基本不变 ,未见动脉粥样硬化形成 ;与高脂模型组相比 ,高脂饲料添加RP组兔血清TC ,TG浓度及LDL C/HDL C比值均显著降低 ,HDL C浓度显著升高 (p <0 .0 5 ) ;LDL C浓度轻度下降 (p >0 .0 5 ) ,主动脉粥样硬化斑块面积和IMT比值也明显降低 (p <0 .0 5 )。 结论菲律宾蛤仔饮食对正常饮食兔血脂和动脉粥样硬化形成无显著影响 ;对高脂饮食兔则能够调节血脂 ,抑制动脉粥样硬化病变形成     

核因子-kB在高脂饮食兔颈总动脉球囊损伤后的动态变化及其与内膜增生的关系

目的观察高脂饮食兔颈总动脉球囊损伤后核因子kB（NF-kB）表达的变化及其与动脉内膜增生的关系。方法对高脂饮食兔颈总动脉球囊损伤后不同时间段的颈总动脉标本采用组织形态学方法检测内膜增生；采用原位杂交方法检测损伤血管NF-kB mRNA的表达。结果（1）球囊损伤后，内膜面积随时间逐步增生，中层各时段均未见明显变化，内膜／中层比率随时间逐步增长。对照侧内膜轻度增生但明显较损伤侧轻（P〈0．05）。（2）球囊损伤后6h即可见NF-kB表达，并于2周达高峰，4周仍有较强表达。NF-kB在损伤侧表达均强于对照侧（P〈0．05）。结论高脂饮食免颈总动脉球囊损伤后，NF-kB被激活，从而引起炎症反应，导致内膜增生可能是再狭窄发生的重要机制之一。     

家兔颈总动脉剥脱术后新生内膜增殖和血管重塑动态变化模型的研究

目的探索再狭窄(RS)的发病机制进行干预研究,复制家兔颈总动脉内膜损伤后不同时间点内膜增殖和血管重塑动态变化模型。方法选用家兔70只行颈总动脉内膜球囊损伤,分别检测未损伤侧(N)和损伤后1d、3d、5d、7d、14d、28d、35 d管腔面积(LA)、内膜和中膜厚度及面积、以及外弹力膜横截面积(EELA)。结果损伤后1d可见动脉内皮剥脱;3d管腔内表面可见增殖的血管平滑肌细胞(VSMC);5~7 d新生内膜(NI)形成并增厚,14 d以后NI厚度及面积逐渐增加,至35 d达最大,同时细胞外基质(ECM)也逐渐增加。损伤后3~14 d中膜厚度及面积逐渐增加,其中14 d中膜面积明显大于N,28~35 d趋于降低。LA于损伤后5~7 d开始减少;14 d以后明显小于N。损伤后1~7 d EELA逐渐增大,至14 d达最大,28 d后开始回缩。结论家兔颈总动脉球囊损伤能较好的模拟RS形成过程,内膜增殖与血管重塑均是RS形成的主要病理机制。     

Nogo‐B expression,in arterial intima,is impeded in the early stages of atherosclerosis in humans

Nogo‐B (Reticulon 4B) is considered to be a novel vascular marker, which may have a protective role in injury‐induced neointima formation and atherosclerosis. Nogo A/B is found to be crucial for monocyte/macrophage recruitment in acute inflammation and it is expressed in CD68 + macrophages. We hypothesize that macrophage infiltration in atherosclerosis is not dependent on Nogo‐B expression in arterial wall. We have assessed Nogo‐B expression and macrophage accumulation in the iliac arteries of healthy organ donors and organ donors with cardiovascular risk factors. Paraffin sections of 66 iliac arteries, from 44 deceased organ donors (17 women and 27 men), were studied. The healthy and cardiovascular risk (CVR) subgroups were created. With regard to staging of the atherosclerotic process, the thickness of arterial intima was measured in digitalized images of H+E stained tissue sections. Immunohistochemical reactions (Nogo‐B and CD68) were carried out in all arteries (66 samples). Western blotting (WB‐19 samples) and real‐time PCR (27 samples) were performed on selected arteries. Significantly higher Nogo‐B expression was demonstrated in the intima of the healthy subjects' subgroup, using immunohistochemistry. WB and real‐time PCR revealed a trend toward lower Nogo‐B expression in the adventitia of the CVR subgroup. Furthermore, the thickness of the intima was found to negatively correlate with the expression of Nogo‐B in the intima and media (r = ?0.32; p < 0.05; r = ?0.32; p < 0.05). Macrophage infiltrates were more prominent in intima of CVR subjects (0.65 vs 3.52 a.u.; p < 0.01). Macrophage density in intima increased with atherosclerosis progression (r = 0.37; p < 0.01). CD68 macrophages density in adventitia was lower in CVR arteries than in healthy arteries. The expression of Nogo‐B, in arterial intima, is impeded in the early stages of atherosclerosis. Accumulation of arterial intimal CD68 macrophages has been shown to progress; however, the overall macrophage density in the adventitia is reduced in arteries shown to have intimal thickening. Macrophage infiltration is not accompanied by Nogo‐B expression in atherosclerotic arteries.     

Assessing Vascular Status and Risk of Latent Ischemia with Ankle Fracture: A Case Report and Algorithm for Treatment

A paucity of published studies and clinical recommendations are available regarding ankle fracture and its association with vascular injury, likely because of the lower incidence relative to the more commonly seen popliteal artery injury after knee dislocation. In the present case report, we describe a previously healthy patient who experienced a pilon type ankle fracture (AO 43C2) with fibular and syndesmotic involvement, followed by a subacute presentation of vascular ischemia weeks after the initial injury and repair, ultimately leading to a major amputation. The failure to identify an occult, vascular injury can have devastating consequences. Guidelines regarding the identification and management of displaced ankle fracture-associated vascular injury, drawing evidence from other traumatic injury complexes, could improve the clinical outcomes. We aim to raise awareness of the association of vascular embarrassment secondary to ankle fracture by proposing a clinical practice algorithm to aid clinicians in recognizing traumatic vascular injury at the earliest and most treatable stage.