新生儿呼吸衰竭时内源性一氧化氮及内皮素的动态观察

目的　了解新生儿呼吸衰竭时内源性一氧化氮（ＮＯ） 和内皮素（ＥＴ） 的动态变化及其在新生儿呼衰的发病中所起的作用。方法　测定了３８ 例新生儿呼衰患儿的尿ＮＯ代谢产物亚硝酸和硝酸根离子（ＮＯ２ － ＋ ＮＯ３ － ＝ ＮＯｘ） 和血浆ＥＴ 水平，同时监测患儿的动态肺顺应性和计算氧合指数（ＯＩ） 。结果　呼吸衰竭的患儿尿ＮＯｘ （２６４．９８±２１８．３２ μｍｏｌ／ｍｇ Ｃｒ） 水平明显降低，血浆ＥＴ（７３ ．０１ ±１０．０６ ｎｇ／Ｌ）水平明显升高，其中的ＲＤＳ组（２０８ ．６４ ±８８．５３ μｍｏｌ／ｍｇ Ｃｒ，８２．３６ ±１７ ．８３ ｎｇ／Ｌ） 变化最为明显。对照组尿ＮＯｘ 和血浆ＥＴ 水平分别为３９７ ．２６ ±２０６ ．６１ μｍｏｌ／ｍｇ Ｃｒ，４０ ．６６ ±１６．８６ ｎｇ／Ｌ。随着疾病的恢复，存活者尿ＮＯｘ 水平上升，而血ＥＴ水平下降，逐渐恢复正常。相关性分析显示尿ＮＯｘ 与ＯＩ呈负相关，与肺顺应性呈正相关，而血ＥＴ与ＯＩ呈正相关，与肺顺应性呈负相关。结论　肺部疾病越重，尿ＮＯｘ 水平越低，血ＥＴ水平越高；严重缺氧所致的内源性ＮＯ合成不足和ＥＴ 合成增加在新生儿呼吸衰竭的发生中可能起了重要的作用。

Observation of intrinsic nitric oxide and endothelin activities in newborns with respiratory failure

Objective To test intrinsic nitric oxide (NO) and endothelin (ET) activities in newborns with respiratory failure. Methods NO oxidation products (NO 2 -+NO 3 =NOx) and creatinine (Cr) were measured daily in the urine of 38 newborns with mechanical ventilation due to respiratory failure. NOx excretion was expressed by urine Cr excretion. Plasma ET was also tested in the patients. Lung compliance was monitored and oxygenation index (OI) was calculated in series. Results Five of the 38 patients developed respiratory distress syndrome. In these patients, urinary NOx (208.64±88.53 μmol/mg Cr) was extremely low while plasma ET was markedly high (82.36±17.83 ng/L). The average value of NOx (264.98±218.32 μmol/mg Cr) was significantly lower while plasma ET (73.01±10.06 ng/L) was higher in all the patients than those seen in the control newborns without pulmonary disease (397.26±206.61 μmol/mg Cr and 40.66±16.86 ng/L). Urinary NOx and plasma ET returned to the normal levels when the patients recovered from respiratory failure. In addition, the lower urinary NOx with the elevated plasma ET was related to the increased OI and to the reduced Lung Compliance. Conclusions Newborn patients with more severe respiratory failure have a lower level of urinary NO oxidation products and a higher level of plasma ET. The results suggest that the decrease of intrinsic NO production and the increase of ET induced by severe hypoxemia may play an important role in the pathogenesis of respiratory failure.