Laser welded vascular anastomosis

Summary A comparative study was undertaken to investigate the application of a specially adapted microsurgical Neodymium Yag Laser system with a wavelength of 1,319 m and a CO₂ laser system for laser assisted microvascular end-to-end anastomosis (LAMA) of the rat femoral artery. Conventionally sutured anastomoses served as controls. Postoperative investigations included patency tests, light microscopy and tensile strength measurements. Both laser systems seem to be equally suitable for LAMA: The patency rates do not differ from those of sutured anstomoses and formation of microscopically small aneurysms occurred predominantly in control animals and only once in laser groups. The clamp time needed for LAMA was half the time that was needed for sutured anastomoses. Wound healing in all groups was similar with less fibrotic reactions and less foreign body granulomas in laser groups. At all intervals tensile strength was significantly higher for sutured anastomoses while differences between the CO₂- and the ND: Yag-laser groups were not statistically significant. Potential applications in urology include microvascular anastomoses in erectile dysfunction, pediatric and reconstructive urology.Contains parts of a dissertation     

踝肱指数和肱踝动脉脉搏波速度与血管舒张功能联合载脂蛋白B与载脂蛋白A-1比值对中青年冠心病血瘀证的预测价值研究

背景 冠心病属中医“胸痹心痛”范畴,其证候分布以血瘀证最为多见,与老年人相比,中青年血瘀证的发生率更高。本研究在团队前期研究基础上进行拓展,首次运用动脉弹性和血管内皮功能检测联合载脂蛋白比值诊断中青年冠心病血瘀证,旨在为早期发现中青年冠心病血瘀证提供新思路,也可为优化补充冠心病血瘀证的诊断标准提供参考。目的 探讨踝肱指数(ABI)、肱踝动脉脉搏波速度(baPWV)、血管舒张功能(FMD)联合载脂蛋白B与载脂蛋白A-1比值(apoB/apoA-1)与中青年冠心病血瘀证的关系及其预测价值。方法 选取2016年12月至2021年12月于中日友好医院中西医结合心脏内科住院治疗的中青年(<50岁)冠心病患者,并根据《冠心病血瘀证诊断标准》分为血瘀证组和非血瘀证组。收集患者首次冠状动脉造影前的ABI、baPWV、FMD和apoB/apoA-1等临床资料。采用多因素Logistic回归分析构建中青年冠心病患者血瘀证的预测模型,并采用受试者工作特征(ROC)曲线进行预测价值评价。结果 本研究共纳入中青年冠心病患者206例,其中血瘀证组127例,非血瘀证组79例。多因素Logistic回归分析结果...     

血管内皮细胞条件培养基促进胃癌细胞增殖和迁移

探讨血管内皮细胞培养基对胃癌细胞增殖和迁移的影响,分析血管内皮细胞调控胃癌细胞发生转移的机制。方法 设置对照组和共培养组,分别将正常培养基和人脐静脉血管内皮细胞HUVEC条件培养基作用于胃癌细胞HGC27,采用MTT法和划痕试验检测胃癌细胞HGC27的增殖活性和迁移能力。设置Control组、6 h组、12 h组和24 h组,以HUVEC的条件培养基作用于胃癌细胞6、12和24 h,Western blot检测EMT标志物和紧密连接蛋白的表达变化,激光共聚焦显微镜观察细胞骨架和紧密连接蛋白的分布变化。结果 MTT及划痕试验表明HUVEC条件培养基促进胃癌细胞HGC27的增殖和迁移。与Control组比较,间接共培养后胃癌细胞的形态呈间充质状改变,丝状伪足样凸起数量显著增加。 Western blot结果显示间接共培养后胃癌细胞上皮标志物E-cadherin表达水平逐渐下降,而间充质标志物N-cadherin和MMP-9逐渐增加,具有时序性变化规律。ZO-1和Occludin的表达也逐渐下降,细胞膜分布减少。结论 间接共培养下,血管内皮细胞通过上调胃癌细胞MMP-9,破坏紧密连接,促进胃癌细胞增殖和迁移     

髓芯减压联合VEGF与胶原基骨移植材料对兔股骨头缺血坏死的修复作用

探讨髓芯减压联合血管内皮生长因子（VEGF）与胶原基骨移植材料对兔股骨头缺血坏死的修复作用。方法 对24只SPF级家兔股骨头内注射无水乙醇建立兔股骨头坏死模型,然后将家兔随机分为模型对照组（A组）、髓芯减压+自体松质骨组（B组）、髓芯减压+胶原基骨修复材料组（C组）和髓芯减压+胶原基骨修复材料+VEGF组（D组）,每组6只,共治疗12周。通过苏木精伊红（HE）染色观察组织切片形态。采用骨密度分析系统（QCT PRO V6.1）测量家兔股骨头骨密度(BMD)。Western blot检测VEGF、Collagen I、Runt相关转录因子2（RUNX2）、骨钙素（OCN）、Wnt-3a、β-catenin和GSK-3β的蛋白表达。结果 术后12周时,与B、C组比较,D组家兔股骨头骨小梁排列较整齐,骨髓中观察到大量微血管的形成,可见明显成骨,且坏死区基本被修复。与A组相比,B组、C组和D组家兔股骨头空骨陷窝比率均显著降低(P＜0.05);D组家兔股骨头空骨陷窝比率小于B组和C组(P＜0.05)。与A组相比,B组、C组和D组家兔股骨头的骨密度均显著升高(P＜0.05);D组骨密度显著高于B组和C组(P＜0.05)。与B组和C组相比,D组VEGF、Collagen I、RUNX2和OCN的蛋白表达水平均显著升高（P＜0.05）;与B组和C组相比,D组Wnt-3a和β-catenin的蛋白表达水平均显著升高,GSK-3β的蛋白表达水平显著降低（P＜0.05）。结论 髓芯减压联合VEGF与胶原基骨移植材料对兔股骨头缺血坏死可有效促进坏死股骨头的修复,提高骨密度及成骨蛋白的表达     

Ultrastructure of capillary walls in human brain tumors

Summary Changes in capillary walls between human glial, non-glial and metastatic brain tumors were studied with conventional ultrathin section and freeze-fracture replica techniques. The following results were obtained. (1) In glial tumors, ultrathin section studies showed cell junctions of the capillaries were either short or elongate. Moreover, endothelial hyperplasia, surface infolding of endothelial cells, irregularity of the basal lamina and a large extravascular space were observed. Freeze-fracture replicas of capillary endothelium showed tight junctions as two to seven strands. In addition, pinocytotic vesicles had increased markedly and were an average of 25 per m². Both ultrathin and freeze fracture studies showed that, in contrast to malignant gliomas, there were only slight changes in benign astrocytomas. (2) In non-glial tumors, ultrathin sections showed surface infoldings, increased vesicles, many fenestrations of endothelial cells, irregularity of basal lamina and enlarged perivascular space. Freeze-fracture replicas of vascular endothelium, showed that the average number of pinocytotic vesicles and fenestrations were 25 and 22 per m², respectively. Moreover, the tight junction was composed of one or two strands which appeared to be a discontinuous array of particles. (3) In metastatic brain tumors, ultrathin studies showed capillary endothelia were proliferated, had marked infolding, and showed an increased number of pinocytotic vesicles and many fenestrations. Moreover, short and elongate intercellular junctions were presented but no open junction was detected. Finally the basal lamina lost its three-layered appearance and was irregular in width. Freeze-fracture replicas showed pinocytotic vesicles had increased and were 24 per m² on average in four cases, but fenestrations and tight junctions could not be detected. The most fundamental feature of vessels in these three different kinds of tumors was whether they were fenestrated or not. Glial tumors were non-fenestrated, whereas non-glial and metastatic tumors were fenestrated.     

Absorption and presystemic glucuronidation of 1-naphthol in the vascularly fluorocarbon emulsion perfused rat small intestine

Summary Using the isolated vascularly fluorocarbon emulsion perfused rat small intestine some factors which determine the extent of the intestinal glucuronidation of 1-naphthol to 1-naphthol--d-glucuronide were studied. Increasing the luminal 1-naphthol concentration resulted in a concomitant increase in the 1-naphthol appearance in the vascular perfusate. In contrast, the total appearance of 1-naphthol--d-glucuronide increased less than proportional to the increase in the luminal 1-naphthol concentration. About 88% of the total amount of 1-naphthol--d-glucuronide excreted was released into the vascular perfusate. The capacity-limited intestinal glucuronide efflux is most likely due to saturation of the excretory mechanism for 1-naphthol--d-glucuronide. Decreasing the vascular flow rate influenced both the appearance of 1-naphthol and 1-naphtol--d-glucuronide in the vascular perfusate, whereas the appearance of 1-naphthol--d-glucuronide in the luminal perfusate was essentially flow-independent. A noradrenaline-induced change in the haemodynamic state of the vascular bed (with the total flow kept constant) resulted in a marked decrease in the 1-naphthol vascular concentration. The vascular 1-naphthol--d-glucuronide concentration was only slightly affected. These results indicate that changes in blood flow and blood flow distribution within the intestinal wall can affect the extent of presystemic intestinal metabolism by interfering with the absorption of the parent compound and the efflux of formed conjugates. These parameters can be of paramount importance for causing variable intestinal first-pass effects of drugs in vivo. Send offprint requests to M. H. de Vries at the above address     

Intermediate filament expression in human vascular smooth muscle and in arteriosclerotic plaques

Summary Different regions of human aorta and of other human arteries obtained at autopsy were analyzed with regard to their topography and to the different stages of arteriosclerosis. Material was studied by immunocytochemical techniques with antibodies specific for either desmin (D) or for vimentin (V), the two types of intermediate filament proteins present in vascular smooth muscle cells. In normal arteries endothelial cells as well as the adjacent intimal cells were D–V+. In the media D+V+ as well as D–V+ cells were present, with the relative numbers of each cell type dependent on the particular blood vessel. When cells in arteriosclerotic plaques at different stages of development were examined an occasional plaque showed cells of the D+V+ type. In the majority of plaques however the cells were V– D+. In plaques where severe ulceration and necrotic material was present D–V+ cells were found at the border of the lesion: foam cells when they could be identified appeared to be D–V+.     

Spectral analysis of spontaneous contractions of the isolated portal vein of rats

Summary The spontaneous contractions of segments of rat portal veins have been examined in vitro under isotonic and isometric conditions. The power density spectra of recorded time series lasting 10–60 min were calculated. The spectra usually consist of harmonic frequency components. Only during shorter periods of analysis (10 min time series) we sometimes found additional non-harmonic components. All frequency components are proportionally shifted by changes of the bath temperature according to an average Q₁₀ of 2.0. Increase of the load decreases the frequency of the contractions.The results of the spectral analysis, indicating a preponderance of a single source of periodicity, were supported by direct evidence of a pacemaker region. By recording contractions after systematic dissections of the portal vein segment, we found that spontaneous activity is generated at the central end of the segment.This work was supported by the Austrian Research Fund     

Differential effects of phosphoramidon and captopril on NK1 receptor-mediated plasma extravasation in the rat trachea

We sought to confirm the identity of the tachykinin receptor subtype that mediates plasma extravasation in the rat trachea, and assess the respective contributions of neutral endopeptidase (NEP) and angiotensin-converting enzyme (ACE) in regulating this tachykinin-induced response. To achieve these aims, we determined the relative potencies of several natural tachykinins and receptor-selective synthetic agonists, both before and after inhibiting NEP with phosphoramidon and ACE with captopril. We also determined the effects of these peptidase inhibitors, and the NK-1 receptor antagonist L-703,606, on the plasma extravasation produced by capsaicin, which releases tachykinins endogenously from sensory nerve endings. We found that the rank order of potency for producing plasma extravasation in the rat trachea was NK-1 receptor agonist ([Sar⁹, Met(O₂)¹¹] SP)>substance P>neurokinin A> neurokinin B. The NK-2 ([Nle¹⁰]NKA (4–10)) and NK-3 ([MePhe⁷]NKB) receptor agonists were without effect. We observed no change in the relative potencies of these peptides after giving rats phosphoramidon or captopril, which suggests that the different peptide potencies are not simply the consequence of different rates of enzymatic degradation. Nevertheless, the responses to substance P and neurokinin A were clearly potentiated in rats given phosphoramidon, indicating that NEP effectively degrades tachykininsin vivo. No significant potentiation was evident for any peptide in rats given captopril. Similarly, the plasma extravasation produced by capsaicin was potentiated in rats given phosphoramidon, but not in those given captopril. Pretreating rats with L-703,606 abolished the response to capsaicin. We conclude from these observations that NK-1 receptors mediate tachykinin-induced plasma extravasation in the rat trachea, and that NEP regulates this response with little or no contribution from ACE.