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目的该研究通过建立大鼠主动脉内皮球囊损伤模型,观察血小板活化、凝血酶受体及血管紧张素Ⅱ1型受体的变化。方法将大鼠随机分为对照组(n=24)和手术组(n=24),并于术后3、7、14和28d取主动脉,通过组织学检查、放射免疫法和反转录聚合酶链反应(RT-PCR)技术检测血管球囊损伤后内膜增生的过程、血小板表面GMP-140的数目、血管AT1受体和凝血酶受体mRNA表达的变化。结果①凝血酶受体mRNA在正常血管组织表达极弱,球囊损伤术后3d已显著增加,术后14d达峰值,术后28d开始下降。②AT1受体mRNA于术后3d明显增高,并持续至术后14d,术后28d恢复至对照水平。③GMP-140于术后3d明显升高,术后7d开始下降。④内皮损伤术后3d已有增殖的血管平滑肌细胞(VSMC)移行至内膜层,术后7d内膜开始增生,术后14dVSMC的增殖及内膜增生更为明显,术后28dVSMC的增殖明显减弱,细胞外基质增加,内膜继续增生。结论血小板活化、凝血酶受体和AT1受体mRNA表达增加参与了血管内皮损伤后内膜增生的过程。
Objective To study the changes of platelet activation, thrombin receptor and angiotensin Ⅱ type 1 receptor in rat aortic endothelial balloon injury model. Methods The rats were randomly divided into control group (n = 24) and operation group (n = 24). The aorta was taken at 3, 7, 14 and 28 days after operation. The histological examination, radioimmunoassay and reverse transcription Polymerase chain reaction (RT-PCR) was used to detect the process of intimal hyperplasia after vascular balloon injury, the number of GMP-140 on platelet surface, the expression of AT1 receptor and thrombin receptor mRNA in blood vessels. Results ① The expression of thrombin receptor mRNA was very weak in normal blood vessels. The volume of thrombin receptor mRNA expression was significantly increased on the 3rd day after balloon injury. The peak value reached the peak on the 14th day and began to decrease after 28 days. ②AT1 receptor mRNA was significantly increased on the 3rd postoperative day, and continued to postoperative 14d, 28d postoperative recovery to the control level. ③GMP-140 increased significantly after 3d, and began to decline 7d after operation. (4) Vascular smooth muscle cells (VSMCs) migrated to the intima layer 3 days after the operation. The intima began to proliferate 7 days after operation. The proliferation and intimal hyperplasia of VSMCs were more obvious on the 14th day after operation, and the proliferation of VSMCs was significantly weakened on the 28th day , Increased extracellular matrix, endometrial continue to proliferate. Conclusion Platelet activation, increased expression of thrombin receptor and AT1 receptor mRNA are involved in intimal hyperplasia after vascular endothelial injury.