冠状动脉旁路移植术后影响静脉移植物内膜增生因素的实验研究

目的　研究静脉移植物内膜增生机理 ,为预防静脉移植物内膜增生寻找合理有效的途径。方法　 2 4只新西兰大白兔随机分为手术组和对照组。应用半定量方法分别于术后 2周、4周检测转化生长因子 β(TGF β)、胶原Ⅰ、胶原Ⅲ和血管紧张素Ⅱ受体 1(AT1R)mRNA表达水平。 结果　手术组各检测指标在各时点均明显高于对照组 (P <0 0 1)。术后 2周时 ,TGF β(4 0 5± 0 4 9vs 2 0 5±0 2 6 ) ;AT1R(18 2 3± 1 32vs 4 6 1± 0 5 3)、胶原Ⅰ (1 80± 0 17vs 0 90± 0 18)、胶原Ⅲ (7 0 5± 0 6 8vs2 80± 0 17)各基因表达水平最高。结论　TGF β、AT1R在内膜增生中可能发挥着重要作用。持续的动脉压力作用是导致TGF β、AT1R大量表达的主要因素 ,并由此导致胶原纤维的大量合成和沉积。

Mechanism of intimal hyperplasia of venous grafts after coronary artery bypass grafting,an experimental study

OBJECTIVE: To study the mechanism of intimal hyperplasia after coronary artery bypass grafting (CABG) and to find an effective way for preventing intimal hyperplasia. METHODS: Twenty-four male New Zealand rabbits were randomly divided into two groups of 12 rabbits: operation group and sham-operation (control) group. The external jugular vein was harvested and anastomosed end-to-side to the ipsilateral carotid artery in operation group or grafted in situ in the control group. Six rabbits in each group were killed and their grafted veins were taken 2 weeks and 4 weeks after operation respectively. The mRNA expressions of transforming growth factor beta (TGF-beta), collagen I, collagen III, and angiotension 1 receptor (AT1R) were measured by RT-PCR and electrophoresis. RESULTS: The intimal hyperplasia was much more remarkable in the operation group than in the control group either 2 weeks or 4 weeks after operation. The mRNA expressions of TGF-beta, AT1R, collagen I, and collagen III were significantly higher in the operation group than in the control group, especially 2 weeks after (P < 0.01). Four weeks after the operation, the expressions of TGF-beta, AT1R, collagen I and collagen III were 4.05 +/- 0.49 vs 2.05 +/- 0.26, 18.23 +/- 1.32 vs 4.61 +/- 0.53, 80 +/- 0.17 vs 0.90 +/- 0.18, and 7.05 +/- 0.68 vs 2.80 +/- 0.17 respectively (all P < 0.05). CONCLUSION: TGF-beta and AT1R may have an important role in the intimal hyperplasia of venous graft in CABG. Continuous arterial pressure may be the main factor of increased expression of TGF-beta and AT1R that cause the enormous synthesis and deposit of collagen.