Vilos G A, Challis J R, Pliagas G A, Lye S L, Possmayer F, Harding P G
Am J Obstet Gynecol. 1985 Oct 15;153(4):472-7. doi: 10.1016/0002-9378(85)90090-0.
We reported previously that metyrapone inhibited the maturational effect of adrenocorticotropin in the fetal sheep lung, even in the presence of exogenous glucocorticoids. To examine the role of beta-adrenergic input in this response we examined lung maturation in fetal sheep treated for 100 hours in vivo with adrenocorticotropin (66 ng/min for 15 minutes every 2 hours, n = 5); adrenocorticotropin plus propranolol (40 micrograms/min, n = 4), or saline solution (n = 8). Pulmonary maturation was assessed by pressure-volume curves, phospholipid content, and morphologic features. The basal cortisol level rose from less than 5 to 32.0 +/- 12.1 and 83.5 +/- 8.0 ng/ml in the adrenocorticotropin and adrenocorticotropin plus propranolol groups, respectively. The adrenal:body weight ratio (X 10(-4)) rose from 1.43 +/- 0.12 in the saline solution group to 2.90 +/- 0.16 and 2.51 +/- 0.14 in the adrenocorticotropin and adrenocorticotropin plus propranolol groups, respectively. Lung distensibility (milliliters of air per gram of lung) rose from 1.10 +/- 0.14 to 1.90 +/- 0.20 in the adrenocorticotropin group but was unchanged (0.98 +/- 0.24) in the adrenocorticotropin plus propranolol group. Phosphatidylcholine (milligrams per gram of lung) in the lung lavage rose from 0.07 +/- 0.02 to 0.23 +/- 0.11 in the adrenocorticotropin group but was not significantly changed (0.12 +/- 0.06) in the adrenocorticotropin plus propranolol group. We conclude that propranolol inhibits the maturational effects of adrenocorticotropin on the fetal lung, which implies that the mechanism of pulmonary maturation is not solely dependent on endogenous cortisol and must be mediated, at least in part, through adrenergic responses.
我们之前报道过，甲吡酮即使在存在外源性糖皮质激素的情况下，也能抑制促肾上腺皮质激素对胎羊肺成熟的作用。为了研究β-肾上腺素能输入在此反应中的作用，我们检测了在体内用促肾上腺皮质激素（每2小时15分钟，66纳克/分钟，n = 5）、促肾上腺皮质激素加普萘洛尔（40微克/分钟，n = 4）或盐溶液（n = 8）处理100小时的胎羊的肺成熟情况。通过压力-容积曲线、磷脂含量和形态学特征评估肺成熟度。促肾上腺皮质激素组和促肾上腺皮质激素加普萘洛尔组的基础皮质醇水平分别从低于5上升至32.0±12.1和83.5±8.0纳克/毫升。肾上腺与体重比（×10⁻⁴）在盐溶液组中从1.43±0.12分别升至促肾上腺皮质激素组的2.90±0.16和促肾上腺皮质激素加普萘洛尔组的2.51±0.14。促肾上腺皮质激素组肺扩张性（每克肺的空气毫升数）从1.10±0.14升至1.90±0.20，但在促肾上腺皮质激素加普萘洛尔组中未改变（0.98±0.24）。肺灌洗中的磷脂酰胆碱（每克肺的毫克数）在促肾上腺皮质激素组中从0.07±0.02升至0.23±0.11，但在促肾上腺皮质激素加普萘洛尔组中无显著变化（0.12±0.06）。我们得出结论，普萘洛尔抑制促肾上腺皮质激素对胎肺的成熟作用，这意味着肺成熟机制并非仅依赖于内源性皮质醇，至少部分必须通过肾上腺素能反应介导。
