Schellenberg J C, Liggins G C, Kitterman J A, Lee C C
Department of Obstetrics and Gynaecology, University of Auckland, New Zealand.
J Appl Physiol (1985). 1993 Jul;75(1):141-7. doi: 10.1152/jappl.1993.75.1.141.
To test whether beta-adrenergic mechanisms and the sympathetic nervous system are involved in the synergistic action of thyrotropin-releasing hormone (TRH) and cortisol on lung maturation, fetal sheep (n = 32) were infused from 121 to 128 days of gestation with saline, TRH + cortisol, TRH + cortisol + beta-adrenergic blocker, or TRH + cortisol after chemical sympathectomy with 6-hydroxydopamine. TRH + cortisol increased lung distensibility and stability and alveolar concentrations of saturated phosphatidylcholine two- to threefold over control fetuses. beta-Adrenergic blockade prevented the increase in distensibility in response to TRH + cortisol. Sympathectomy did not impair the increase in distensibility and stability in response to TRH + cortisol but inhibited the increase in alveolar total phospholipids. Tissue concentrations of saturated phosphatidylcholine increased in TRH + cortisol-treated fetuses after either sympathectomy or beta-adrenergic blockade. We concluded that during lung maturation by TRH + cortisol 1) sympathetic mechanisms are requisite for surfactant release, 2) nonneurogenic beta-adrenergic mechanisms are requisite for the maturation of the mechanical properties of the lung and 3) stimulation of surfactant synthesis is independent of beta-adrenergic action and the sympathetic nervous system.
为了测试β-肾上腺素能机制和交感神经系统是否参与促甲状腺激素释放激素（TRH）和皮质醇对肺成熟的协同作用，在妊娠121至128天期间，给32只胎羊输注生理盐水、TRH + 皮质醇、TRH + 皮质醇 + β-肾上腺素能阻滞剂，或在经6-羟基多巴胺进行化学交感神经切除术后输注TRH + 皮质醇。与对照胎儿相比，TRH + 皮质醇使肺扩张性、稳定性及饱和磷脂酰胆碱的肺泡浓度增加了两到三倍。β-肾上腺素能阻滞可防止因TRH + 皮质醇引起的扩张性增加。交感神经切除并不损害对TRH + 皮质醇的扩张性和稳定性增加，但抑制了肺泡总磷脂的增加。在交感神经切除或β-肾上腺素能阻滞后，TRH + 皮质醇处理的胎儿组织中饱和磷脂酰胆碱浓度增加。我们得出结论，在TRH + 皮质醇促进肺成熟过程中：1）交感机制是表面活性剂释放所必需的；2）非神经源性β-肾上腺素能机制是肺机械性能成熟所必需的；3）表面活性剂合成的刺激独立于β-肾上腺素能作用和交感神经系统。
