Khomeriki S G, Zhukov A G
Arkh Patol. 2011 Jul-Aug;73(4):43-7.
The pathogenesis of portal hypertension (PH) involves venous congestion with gastric mucosal capillary dilatation. The formation of new blood vessels, as was shown in experimental models of PH, is pathological hallmark of PH. Generation of new blood vessels is stimulated by vascular endothelial growth factor (VEGF), the regulator of angiogenesis. The aim of the study was to investigate changes in gastric microvessels in patients with liver cirrhosis complicated with PH in different stages, and the factors influencing the development of portal hypertensive gastropathy. We studied the relation between gastric mucosal capillary parameters, measured morphometrically, and endoscopic appearances in 56 patients with PH. The gastric biopsy was obtained from antrum and corpus of the stomach. We determined expression and localization of Fit-1 receptor for VEGF in human gastric mucosa by immunohistochemistry. Mucosal capillary network assessed on histological sections immunostained for CD34, a specific marker for endothelial cells and revealed proliferating endothelial cells by Ki-67 antibodies. Nicon CP 995 camera and digital image analyzing system (DMI-1) was used for morphometry. The number, size and relative volume of vessels in gastric mucosa were evaluated. Helicobacter pillory-positive patients were excluded from study. The number of vessels in gastric mucosa was significantly higher in groups with PH (p < 0.05) compared with patients without PH. The mean size of vessels in gastric mucosa was decreased in patients with PH (212 +/- 20 vs 282 +/- 25 mkm2, p < 0.05) in atrum and (155 +/- 12 vs 198 +/- 13 mkm2, p < 0.039) in corpus. The majority of the vessels were presented by newly formed small sized capillaries. Meanwhile the relative volume of vessels in gastric mucosa was not changed significantly in groups with PH. These observations have not supported the view that PH is usually associated with a prominent dilatation of gastric mucosal capillaries. Our data have shown intensifying of neoangiogenesis in human gastric mucosa at PH. The anti-angiogenic therapeutic approach could be taken into consideration for patients suffering from PH.
门静脉高压症（PH）的发病机制涉及静脉充血伴胃黏膜毛细血管扩张。正如在PH实验模型中所显示的，新血管的形成是PH的病理标志。血管内皮生长因子（VEGF）作为血管生成的调节因子，可刺激新血管的生成。本研究的目的是调查不同阶段肝硬化合并PH患者胃微血管的变化，以及影响门静脉高压性胃病发展的因素。我们研究了56例PH患者经形态学测量的胃黏膜毛细血管参数与内镜表现之间的关系。胃活检取自胃窦和胃体。我们通过免疫组织化学法测定人胃黏膜中VEGF的Fit-1受体的表达和定位。在免疫染色为CD34（内皮细胞特异性标志物）的组织切片上评估黏膜毛细血管网络，并用Ki-67抗体显示增殖的内皮细胞。使用尼康CP 995相机和数字图像分析系统（DMI-1）进行形态测量。评估胃黏膜中血管的数量、大小和相对体积。幽门螺杆菌阳性患者被排除在研究之外。与无PH的患者相比，PH组胃黏膜中的血管数量明显更高（p < 0.05）。PH患者胃窦部胃黏膜中血管的平均大小减小（212 +/- 20 vs 282 +/- 25μm²，p < 0.05），胃体部为（155 +/- 12 vs 198 +/- 13μm²，p < 0.039）。大多数血管是新形成的小尺寸毛细血管。同时，PH组胃黏膜中血管的相对体积没有明显变化。这些观察结果不支持PH通常与胃黏膜毛细血管显著扩张相关的观点。我们的数据表明，在PH时人胃黏膜中的新生血管生成增强。对于患有PH的患者，可以考虑采用抗血管生成治疗方法。
