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目的观察宫内炎性暴露对早产大鼠支气管肺泡灌洗液内血管内皮生长因子及其受体含量的影响,探讨其与新型支气管肺发育不良发病机制之间的关系。方法定期受孕的Sprague Dawley(SD)大鼠随机分为脂多糖(LPS)组和生理盐水组(对照组),于孕15d羊膜腔内注射LPS/无菌生理盐水。两组动物均于出生后第1d(P1)、3d(P3)、5d(P5)和7d(P7)各随机取8只,应用ELISA方法检测BALF中VEGF及其受体的含量。结果LPS组随鼠龄递增,VEGF含量逐渐增加,P7达高峰。与对照组相比,LPS组在P1显著低于对照组(P<0.05);在P5明显高于对照组,并且差异有统计学意义(P<0.05)。其受体Flk-1的含量变化规律与其基本类似。结论宫内炎性暴露可通过调控VEGF及其受体的含量,引起肺微血管发生病理性重塑,肺泡化过程受阻,进而导致BPD的发生。
Objective To observe the effect of intrauterine inflammatory exposure on the content of vascular endothelial growth factor and its receptor in bronchoalveolar lavage fluid in preterm rats and explore the relationship between it and the pathogenesis of new bronchopulmonary dysplasia. Methods Sprague Dawley rats were randomly divided into LPS group and normal saline group (control group). LPS / sterile saline was injected into the amniotic cavity 15 days after pregnancy. Eight rabbits were randomly selected from the first day (P1), the third day (P3), the fifth day (P5) and the seventh day after birth (P7). The contents of VEGF and its receptor in BALF were detected by ELISA. Results With the increasing of age, the content of VEGF gradually increased and the peak of P7 reached the peak in LPS group. Compared with the control group, LPS group in P1 was significantly lower than the control group (P <0.05); P5 was significantly higher than the control group, and the difference was statistically significant (P <0.05). Its receptor Flk-1 content changes with its basic similarities. Conclusions Intrauterine inflammatory exposure can cause pathological remodeling of pulmonary microvessels and obstruct the process of alveolar inflammation by regulating the content of VEGF and its receptor, leading to the occurrence of BPD.