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目的 :探讨组织肾素 -血管紧张素系统 ( RAS)在血管球囊损伤后内膜增生中的作用。方法 :用放射免疫法测定血管球囊损伤后大鼠的血浆肾素活性 ( RA)、血管紧张素 ( Ang ) ;用生物化学方法检测血清和组织血管紧张素转换酶 ( ACE)活性 ;免疫组化法观察血管壁细胞增殖过程。结果 :损伤后循环中 RAS各成分无明显变化 ,球囊损伤后第 3天组织中 ACE活性增高 ( P <0 .0 1) ,第 14天达最高 ,第 2 8天降至基础水平。ACE活性与 PCNA阳性细胞数呈正相关。ACE抑制剂 Perindopril抑制组织中 ACE活性 ,减少内膜增生。结论 :组织 RAS而非循环 RAS在血管球囊损伤后内膜增生中起重要作用。通过抑制组织 ACE活性可以预防血管成形术后再狭窄。
Objective: To investigate the role of tissue renin-angiotensin system (RAS) in neointimal hyperplasia after vascular balloon injury. Methods: The plasma renin activity (RA) and angiotensin (Ang) were measured by radioimmunoassay in rats; the serum and tissue ACE activity were measured by biochemistry method; Method to observe the proliferation of vascular wall cells. Results: There was no significant change of RAS in the circulation after injury. The activity of ACE in the third day after balloon injury increased (P <0.01), reached the highest on the 14th day and dropped to the basal level on the 28th day. ACE activity and PCNA positive cells was positively correlated. ACE inhibitor Perindopril inhibits ACE activity in tissues and reduces intimal hyperplasia. Conclusion: Tissue RAS but not circulatory RAS play an important role in neointimal hyperplasia after vascular balloon injury. Restenosis after angioplasty can be prevented by inhibiting tissue ACE activity.