先天性膈疝动物模型制作及其肺部一氧化氮的改变

Preparation of neonatal rat models with congenital diaphragmatic hernia and change of nitric oxide level in lungs of the models

用Nitrofen致畸孕鼠,获取先天性膈疝鼠仔模型。共获得28只先天性膈疝(CDH)鼠仔,经Nitrofen处理未患CDH鼠仔34只,正常对照组鼠仔25只。对3组进行肺重/体重指数、肺蛋白定量、肺中一氧化氮合成酶(NOS)和一氧化氮(NO)研究。结果发现用Nitrofen致畸孕鼠,在鼠仔中能产生CDH;病侧肺组织中NO含量下降,NOS酶活性下降。由于NO能舒张血管平滑肌细胞,因此病侧肺组织中NO含量明显下降,和CDH肺高压病理生理有关。NO制剂是治疗CDH肺高压一种有希望的新途径。

10 timed-pregnant rats were fed Nitrofen. a herbicide, to induce the formation of congenital diaphragmatic hernia(CDH) in their neonatal rats. CDH was successfully created in 28 neonatal rats as group Ⅰ, and 34 neonatal rats without CDH formation were as group Ⅱ among 62 neonatal rats of Nitrofen-administrated maternal rats. There were other 25 normal neonatal rats as control group. All neonatal rats were killed at second day after birth. The lung weight/body weight index, the activity of NO synthetase (NOS) and the level of nitric oxide (NO)in lungs were measured in three groups. The results showed that the lung weight/body weight index in the group I decreased evidently comparing to that in the control group(19. 29±4. 35 VS. 26. 76±8. 3). The activity of NOS and the level of NO decreased significantly in the unilateral lung with CDH. It is suggested that prenatal Nitrofen administration can induce CDH formation in neonatal rat. NO deficiency in the unilateral lung with CDH can be probably correlated with the existence of pulmonary hypertension induced by CDH since NO can dilate smooth muscle cell of the pulmonary vessels. NO will be hopeful for the treatment of pulmonary hypertension in CDH patients.