AngⅡ诱导的VEGF对食用蛙心包淋巴孔和间皮血窦的影响

ANGIOTENSIN Ⅱ-INDUCED VASCULAR ENDOTHELIAL GROWTH FACTOR REGULATES PERICARDIAL LYMPHATIC STOMATA AND MESOTHELIAL SINUSOID IN EUROPEAN EDIBLE FROG (RANA ESCULENTA)

血管紧张素Ⅱ (angiotensinⅡ ,AngⅡ )在许多血管性疾病中发挥了重要作用。本文研究AngⅡ对血管内皮细胞生长因子 (vascularendothelialgrowthfactor,VEGF)调控蛙心包淋巴孔和心包间皮血窦的影响。选用食用蛙 (Ranaesculenta)进行本项目研究。应用AngⅡ +VEGF和VEGF蛙腹膜腔注射 ,扫描电镜观察和计算机图像处理。正常蛙心包壁层有一些散在分布的心包淋巴孔和少量间皮血窦。VEGF组的淋巴孔直径、分布密度和间皮血窦面积分别是 1 5 0 μm、 8 2 5 / 0 1mm2 和 2 44 3 95 μm2 / 0 1mm2 均高于对照组 (P <0 0 1)。AngⅡ对VEGF有明显诱导作用 ,使淋巴孔直径 (2 81μm)、分布密度 (2 8 82 / 0 1mm2 )和血窦面积 (386 6 15 μm2 /0 1mm2 )高于VEGF组 ,两者有显著差异 (P <0 0 5 )。VEGF可使蛙心包淋巴孔开放数量增多 ,孔径开大 ,分布密度增高 ,具有明显调控心包淋巴孔的功能 ;此外 ,还能使心包间皮血窦面积增多 ,进而使心包间皮通透性增加。AngⅡ能促进VEGF的作用 ,这对于加速心包腔内物质转归 ,促进心包膜漏出 ,防止心肌间质水肿有重要作用。结果提示 ,AngⅡ对VEGF的诱导作用可能是通过增加VEGF基因的表达而实现。

Angiotensin Ⅱ (AngⅡ) plays a role in many vascular diseases. In the present study, the effect of AngⅡ on vascular endothelial growth factor (VEGF) regulating the pericardial lymphatic stomata and the pericardial mesothelium was investigated in the European edible frog (Rana esculenta). AngⅡ+VEGF and VEGF were injected into the peritoneal cavity in 10 frogs respectively. The results were obtained by using scanning electron microscopy and computerized imaging analysis. Scatteredly distributed pericardial lymphatic stomata were found on the parietal pericardium with a few mesothelial sinusoid in the frogs. In the VEGF group, which consisted of 5 frogs, the average diameter of the stomata, the average distribution density of the stomata and the sinusoid areas were 1 50 μm, 8 25/0 1 mm 2 and 2 443 95 μm 2/0 1 mm 2 respectively, which were much higher than those in control group ( P <0 01). AngⅡ induced a significant increase of the effects of VEGF on the stomata diameter (2 81 μm), the stomata distribution density (28 82/0 1 mm 2) and the sinusoid areas (3 866 14 μm 2/0 1 mm 2), which were much higher than those in the VEGF group ( P <0 05). VEGF strongly regulated the pericardial lymphatic stomata by increasing their numbers, diameters, and higher distribution density and also increased the sinusoid area with the result of the higher permeability of the pericardium. AngⅡ enhanced VEGF induced the stomata and the sinusoid, which would speed up material transfer of the pericardipal cavity and pericardial leaking from the myocardium so as to play an important role in preventing myocardial interstitial edema. These findings suggest that AngⅡ may potentiate VEGF induced regulatory activity of the pericardial lymphactic stomata and sinusoid through a increase in the gene expression of VEGF.