| 1. | The intima of the bridged arterial segment is generally spared from atherosclerosis
心肌架桥处的血管内膜常可免于粥状硬化。 |
| 2. | Could this drug effect vascular intima thickness ? is there any direct evidence
这些药物会影响血管内膜厚度吗？是否有直接的证据？ |
| 3. | Removal of the noise in exercise electrocardiogram signals using selfadaptive signal enhancer based on neural network
新型血管吻合用支架对血管内膜的影响 |
| 4. | Non active surgical implants . particular requirements for cardiac and vascular implants . part 3 : endovascular devices
非活动外科植入物.血管和心脏植入物的特殊要求.第3部分:血管内膜设备 |
| 5. | Results : the fundamental pathological changes were the endoangiitis and an infiltration usually containing a significant admixture of plasma cells
结果：基本病理改变为血管内膜炎和以浆细胞为主的混合型炎细胞浸润。 |
| 6. | These patients underwent ultrasound assessment of the major artery ( carotid artery ) for the thickness of atherosclerotic plaque , or carotid intimomedial thickness ( imt )
患者亦会接受颈动脉血管超声波检查，以量度血管粥样斑块及血管内膜中层的厚度。 |
| 7. | Anti - inflammatory agents and immunomodulators , antiproliferative agents , inhibitors of smooth muscle cell proliferation and migration , accelerant of endothelialization of injury - artery , etc . are drugs have been mostly studied nowadays
抗炎症和免疫调节药物、抗增殖药物、抑制血管平滑肌细胞迁移的药物、促进损伤血管内膜内皮化的药物等是目前研究较多的药物。 |
| 8. | Proliferation of vascular smooth muscle cells is involved not only in the process of pulmonary hypertension but also in many other vascular diseases such as atherosclerosis and restenosis after angioplasty or coronary artery bypass grafting ( cabg )
Vsmcs的异常增殖除了参与肺动脉高压的形成，还与动脉粥样硬化、血管成形术后再狭窄过程中血管内膜的增厚关系密切， vnp对肺动脉之外的其它血管平滑肌的异常增殖是否有调节作用尚无报道。 |
| 9. | Conclusion one mechanism of wmt on aso may be its inhibition on arteriosclerosis by way of downregulating the expression of vascular endothelial cells adhesion molecules to decrease the adhesion of monocyte to vec , therefore to inhibit the monocytes migrating into vascular intima to develop foam cells
结论下调血管内皮细胞黏附分子的表达，减少单核细胞与内皮细胞的黏附，从而抑制单核细胞迁移至血管内膜形成泡沫细胞，抑制动脉粥样硬化as的形成，可能是温脉通治疗aso的机制之一。 |
| 10. | Conclusion one mechanism of wmt on aso may be its inhibition on arteriosclerosis by way of downregulating the expression of vascular endothelial cells adhesion molecules to decrease the adhesion of monocyte to vec , therefore to inhibit the monocytes migrating into vascular intima to develop foam cells . 2007 vol
结论下调血管内皮细胞黏附分子的表达，减少单核细胞与内皮细胞的黏附，从而抑制单核细胞迁移至血管内膜形成泡沫细胞，抑制动脉粥样硬化as的形成，可能是温脉通治疗aso的机制之一。 |
