尾加压素Ⅱ对大鼠胸主动脉球囊损伤后血管重塑的作用

目的： 探讨尾加压素Ⅱ(UII)在血管损伤后重塑过程中的作用。方法: 建立大鼠胸主动脉球囊拉伤模型，随机分为4组（n=5）,分别为假拉伤组、拉伤组、UII组（胸主动脉球囊拉伤并持续泵入UII 1.0 nmol·kg-1·h-1）和urantide组( 胸主动脉球囊拉伤并持续泵入urantide 10 nmol·kg-1·h-1)。于第21 d取胸主动脉，分别检测血管形态改变、UII表达、平滑肌细胞增殖和胶原表达。结果: ①术后第21 dUII组收缩压高于拉伤组［（140.0±10.0) mmHg vs (132.0±3.4) mmHg, P>0.05］,明显高于urantide 组［（140.0±10.0) mmHg vs (128.0±2.4) mmHg, P<0.05］。②胸主动脉球囊损伤后,损伤血管局部UII表达增强。③同拉伤组比, UII组进一步促进了内膜的增生,管腔面积狭窄率明显增加(0.13±0.05 vs 0.07±0.02, P<0.05);细胞增殖指数明显增加(0.74±0.16 vs 0.40±0.11,P<0.01);胶原表达也明显增加(以IOD计量,318±127 vs 78±26, P<0.01)。④同拉伤组比,urantide组管腔面积狭窄率没有减轻(0.09±0.03 vs 0.07±0.02, P>0.05);细胞增殖指数明显增加(0.73±0.15 vs 0.40±0.11, P<0.01);胶原表达增多但无统计学意义(以IOD计量,200±79 vs 78±26, P>0.05)。结论: 大鼠胸主动脉损伤后局部UII表达增强；外源性UII促进新生内膜平滑肌细胞增殖和胶原表达，加重了损伤血管的狭窄，提示UII参与了损伤后修复的过程；10 nmol·kg-1·h-1urantide不能抑制损伤后血管重塑的进程, 拮抗UII的机制尚有待进一步探讨。

Role of vascular remodeling for urotensin Ⅱ in rat thoracic aorta after balloon injury

AIM: To explore the possible effect of UII in the process of remodeling after vascular injury. METHODS: The rat model of balloon injury in thoracic aorta was established. Male rats were randomized to 4 groups (n=5), including sham injury group, injury group, UII group (UII pumped into the rats after thoracic aorta balloon injury at 1.0 nmol·kg-1·h-1) and urantide group (urantide pumped into the rats after thoracic aorta balloon injury at 10 nmol·kg-1·h-1). At 21 days, the thoracic aortas were taken out to measure the changes of pathology, the expression of UII, the proliferation of VSMC and the expression of collagen. RESULTS: (1) At the 21 days after operations, the systolic blood pressure was higher in UII group than that in injury group ［(140.0±10.0) mmHg vs (132.0±3.4) mmHg, P>0.05］. The systolic blood pressure was also obviously higher than that in urantide group ［(140±10.0) mmHg vs (128.0±2.4) mmHg, P<0.05］. (2) Urotensin Ⅱ was expressed strongly in the injured area after thoracic aorta injury. (3) In contrast to injury group, the intimal thicken in urotensin Ⅱ group enhanced, the decrease in lumen area was marked (0.13±0.05 vs 0.07±0.02, P<0.05), the cell proliferation index was markedly increased (0.74±0.16 vs 0.40±0.11, P<0.01), and the expression of collagen was also markedly increased (counted as IOD, 318±127 vs 78±26, P<0.01). (4) In contrast to injury group, the decrease in lumen area was not abolished (0.09±0.03 vs 0.07±0.02, P>0.05) after chronic infusion of urotensin Ⅱ receptor antagonist urantide, the cell proliferation index was markedly increased (0.73±0.15 vs 0.40±0.11, P<0.01) and the expression of collagen was not statistically increased (counted as IOD, 200±79 vs 78±26, P>0.05). CONCLUSION: Urotensin Ⅱ expresses strongly in the myointimal cells after thoracic aorta injury in rat. The extra UII enhances the proliferation of VSMC and expression of collagen in the myointimal, increases the stenosis of injured vasculature, indicating that UII might take part in the process of repairing after vessel injury.